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    R&D Systems il 17
    <t>TNFα+IL-17</t> induces pendrin coexpression with CFTR in secretory cells but not in ionocytes. Human airway epithelia were treated with TNFα+IL-17 for 48 h. A and B : pendrin was coexpressed with CFTR. A shows an en face projection, and B shows an X-Z projection. C and D : CFTR-expressing cells were CC10+ secretory cells. C shows an en face projection, and D shows an X-Z projection. E : colocalization of CFTR with pendrin and CC10 markers measured using the ImageJ software and reported as Pearson’s correlation coefficient r ( n = 3–5). F and G : ionocytes were identified by labeling with BSND (Barttin) antibodies. Ionocytes showed CFTR labeling but lacked significant pendrin labeling. Scale bars: A and C , 10 μm; B , D , E , and F , 5 μm. H : quantification of CFTR or pendrin expression in BSND+ cells. BSND+ cells from CFTR- or pendrin-labeled epithelia were shown in a blinded fashion to 3 investigators experienced in confocal microscopy of airway epithelia. Investigators graded intensity of apical protein (CFTR or pendrin) expression on a scale: none or low = 1, moderate = 2, high = 3. Bars indicate means ± SD. **** P
    Il 17, supplied by R&D Systems, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17/product/R&D Systems
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17 - by Bioz Stars, 2021-06
    86/100 stars
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    86
    Thermo Fisher il 17a
    Proposed mechanisms of acute kidney injury induced liver dysfunction and systemic inflammation Acute kidney injury causes small intestinal generation of <t>IL-17A</t> and subsequent intestinal injury (villous endothelial apoptosis, epithelial necrosis, increased pro-inflammatory cell translocation and cytokine flux to the liver). These events cause hepatic injury (inflammation, apoptosis and necrosis) with increased generation and release of TNF-α and IL-6 systemically causing further multi-organ injury and systemic inflammation.
    Il 17a, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17a/product/Thermo Fisher
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17a - by Bioz Stars, 2021-06
    86/100 stars
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    88
    BioLegend il 17a
    Reduced CD4 + Foxp3 + Treg in L. sigmodontis -infected <t>IL-17A</t> −/− C57BL/6 mice at the site of infection. On day 28 of infection, thoracic ( a , b ) and mLN ( c , d ) cell populations were screened for levels of CD4 + T cells ( a , c ) and CD4 + Foxp3 + Treg ( b , d ) populations. Values are expressed as mean ± SEM and symbols show levels in each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p
    Il 17a, supplied by BioLegend, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17a/product/BioLegend
    Average 88 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17a - by Bioz Stars, 2021-06
    88/100 stars
      Buy from Supplier

    86
    Becton Dickinson il 17a
    Reduction of the lesion size in the lungs of <t>IL‐17A</t> KO mice after M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. The mice were sacrificed 30, 60, and 120 days after infection, and formalin‐fixed sections were stained with hematoxylin and eosin. Representative lung tissue specimens from the wild‐type C57BL/6 mice (left panel) and the IL‐17A KO mice (right panel) are shown. Magnification, ×40 (A), ×400 (B).
    Il 17a, supplied by Becton Dickinson, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il 17a/product/Becton Dickinson
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    il 17a - by Bioz Stars, 2021-06
    86/100 stars
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    Interleukin 17A IL17A is also known as cytotoxic T lymphocyte associated antigen 8 CTLA8 which is a proinflammatory cytokine produced by activated T cells IL17A can regulate the activities of
      Buy from Supplier

    N/A
    IL 17 was identified from a CD4 T cells DNA library IL 17 can be induced from primary peripheral blood CD4 T cells upon stimulation The cytokine exhibits a high
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    Anti IL 17 RABBIT Antibody 600 401 BU7
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    N/A
    The IL 17 RA IL 17 R Antibody from Novus Biologicals is a goat polyclonal antibody to IL 17 RA IL 17 R This antibody reacts with rat The IL
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    Image Search Results


    TNFα+IL-17 induces pendrin coexpression with CFTR in secretory cells but not in ionocytes. Human airway epithelia were treated with TNFα+IL-17 for 48 h. A and B : pendrin was coexpressed with CFTR. A shows an en face projection, and B shows an X-Z projection. C and D : CFTR-expressing cells were CC10+ secretory cells. C shows an en face projection, and D shows an X-Z projection. E : colocalization of CFTR with pendrin and CC10 markers measured using the ImageJ software and reported as Pearson’s correlation coefficient r ( n = 3–5). F and G : ionocytes were identified by labeling with BSND (Barttin) antibodies. Ionocytes showed CFTR labeling but lacked significant pendrin labeling. Scale bars: A and C , 10 μm; B , D , E , and F , 5 μm. H : quantification of CFTR or pendrin expression in BSND+ cells. BSND+ cells from CFTR- or pendrin-labeled epithelia were shown in a blinded fashion to 3 investigators experienced in confocal microscopy of airway epithelia. Investigators graded intensity of apical protein (CFTR or pendrin) expression on a scale: none or low = 1, moderate = 2, high = 3. Bars indicate means ± SD. **** P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: TNFα+IL-17 induces pendrin coexpression with CFTR in secretory cells but not in ionocytes. Human airway epithelia were treated with TNFα+IL-17 for 48 h. A and B : pendrin was coexpressed with CFTR. A shows an en face projection, and B shows an X-Z projection. C and D : CFTR-expressing cells were CC10+ secretory cells. C shows an en face projection, and D shows an X-Z projection. E : colocalization of CFTR with pendrin and CC10 markers measured using the ImageJ software and reported as Pearson’s correlation coefficient r ( n = 3–5). F and G : ionocytes were identified by labeling with BSND (Barttin) antibodies. Ionocytes showed CFTR labeling but lacked significant pendrin labeling. Scale bars: A and C , 10 μm; B , D , E , and F , 5 μm. H : quantification of CFTR or pendrin expression in BSND+ cells. BSND+ cells from CFTR- or pendrin-labeled epithelia were shown in a blinded fashion to 3 investigators experienced in confocal microscopy of airway epithelia. Investigators graded intensity of apical protein (CFTR or pendrin) expression on a scale: none or low = 1, moderate = 2, high = 3. Bars indicate means ± SD. **** P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Expressing, Software, Labeling, Confocal Microscopy

    CFTR contributes to TNFα+IL-17-induced airway surface liquid (ASL) alkalinization. A : after TNFα+IL-17 treatment for 24 h, human airway epithelia were treated for 2 h with either apical vehicle (DMSO) or CFTR(inh)-172 suspended in a volatile solvent (Fluorinert FC-72) to achieve an approximate ASL concentration of 10 μM. pH of ASL (pH ASL ) was measured with SNARF-1-dextran in the presence of HCO 3 − /CO 2 ( n = 6). B and C : effect of negative control (NC) or siRNA directed against CFTR on pH ASL in vehicle- or TNFα+IL-17-treated epithelia ( n = 5). Each data point represents epithelium from a different donor. Bars indicate means ± SD. Data were analyzed using repeated measures ANOVA with Tukey’s multiple comparisons test ( A ) or paired Student’s t test ( B and C ). * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: CFTR contributes to TNFα+IL-17-induced airway surface liquid (ASL) alkalinization. A : after TNFα+IL-17 treatment for 24 h, human airway epithelia were treated for 2 h with either apical vehicle (DMSO) or CFTR(inh)-172 suspended in a volatile solvent (Fluorinert FC-72) to achieve an approximate ASL concentration of 10 μM. pH of ASL (pH ASL ) was measured with SNARF-1-dextran in the presence of HCO 3 − /CO 2 ( n = 6). B and C : effect of negative control (NC) or siRNA directed against CFTR on pH ASL in vehicle- or TNFα+IL-17-treated epithelia ( n = 5). Each data point represents epithelium from a different donor. Bars indicate means ± SD. Data were analyzed using repeated measures ANOVA with Tukey’s multiple comparisons test ( A ) or paired Student’s t test ( B and C ). * P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Concentration Assay, Negative Control

    SLC26A4 (pendrin) contributes to TNFα+IL-17-induced airway surface liquid (ASL) alkalinization. A and B : siRNA directed against SLC26A4 was used to knock down expression, and pH of ASL (pH ASL ) was measured after treatment with either vehicle or TNFα+IL-17 for 24 h ( n = 6). Individual data points in each group represent epithelia from a different donor. Bars indicate means ± SD. Groups were compared with paired Student’s t test. * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: SLC26A4 (pendrin) contributes to TNFα+IL-17-induced airway surface liquid (ASL) alkalinization. A and B : siRNA directed against SLC26A4 was used to knock down expression, and pH of ASL (pH ASL ) was measured after treatment with either vehicle or TNFα+IL-17 for 24 h ( n = 6). Individual data points in each group represent epithelia from a different donor. Bars indicate means ± SD. Groups were compared with paired Student’s t test. * P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Expressing

    Gene expression profiling identifies SLC26A4 (pendrin) as a key non-CFTR HCO 3 − transporter upregulated by TNFα+IL-17. Human airway epithelia were treated with vehicle or TNFα+IL-17 for 48 h, and RNA-sequencing was performed ( n = 6 different donors). A : volcano plot shows TNFα+IL-17-induced gene expression changes. Each data point corresponds to a gene. A horizontal dashed line labeled 0.05 represents arbitrary cutoff of adjusted P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: Gene expression profiling identifies SLC26A4 (pendrin) as a key non-CFTR HCO 3 − transporter upregulated by TNFα+IL-17. Human airway epithelia were treated with vehicle or TNFα+IL-17 for 48 h, and RNA-sequencing was performed ( n = 6 different donors). A : volcano plot shows TNFα+IL-17-induced gene expression changes. Each data point corresponds to a gene. A horizontal dashed line labeled 0.05 represents arbitrary cutoff of adjusted P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Expressing, RNA Sequencing Assay, Labeling

    TNFα+IL-17 increase pendrin expression. Human airway epithelia were treated with either vehicle or TNFα+IL-17 for 48 h. A and B : confocal images show immunostaining for pendrin (green) and actin (phalloidin, red) in control ( A ) and TNFα+IL-17-treated epithelia ( B ). Scale bar, 10 μm. C : intensity of pendrin immunolabeling measured as integrated density using the ImageJ software ( n = 5). ** P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: TNFα+IL-17 increase pendrin expression. Human airway epithelia were treated with either vehicle or TNFα+IL-17 for 48 h. A and B : confocal images show immunostaining for pendrin (green) and actin (phalloidin, red) in control ( A ) and TNFα+IL-17-treated epithelia ( B ). Scale bar, 10 μm. C : intensity of pendrin immunolabeling measured as integrated density using the ImageJ software ( n = 5). ** P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Expressing, Immunostaining, Immunolabeling, Software

    TNFα+IL-17 induce pendrin expression mainly in secretory cells. Human airway epithelia were treated with TNFα+IL-17 for 48 h. A and B : ciliated cells lacked significant pendrin expression. A shows an en face projection, and B shows an X-Z projection. C and D : pendrin-expressing cells were, in many cases, CC10+, which labels secretory cells. C shows an en face projection, and D shows an X-Z projection. Scale bars: A and C , 10 μm; B and D , 5 μm. E : colocalization of pendrin with ciliated cell and CC10 markers measured using the ImageJ software and reported as Pearson’s correlation coefficient r ( n = 5–7).

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: TNFα+IL-17 induce pendrin expression mainly in secretory cells. Human airway epithelia were treated with TNFα+IL-17 for 48 h. A and B : ciliated cells lacked significant pendrin expression. A shows an en face projection, and B shows an X-Z projection. C and D : pendrin-expressing cells were, in many cases, CC10+, which labels secretory cells. C shows an en face projection, and D shows an X-Z projection. Scale bars: A and C , 10 μm; B and D , 5 μm. E : colocalization of pendrin with ciliated cell and CC10 markers measured using the ImageJ software and reported as Pearson’s correlation coefficient r ( n = 5–7).

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Expressing, Software

    TNFα+IL-17 increase CFTR activity and expression. After TNFα+IL-17 treatment for 24 h, human airway epithelia were mounted in modified Ussing chambers with symmetric Krebs-Ringer solution gassed with 5% CO 2 . Epithelia were voltage clamped followed by continuous recording of short-circuit current ( I SC ) and transepithelial conductance ( G t ) as pharmacologic agents were sequentially added to the apical chamber. A – D : I SC , Δ I SC , G t , and Δ G t in control and TNFα+IL-17-treated epithelia. E : TNFα+IL-17-induced changes in SCNN1A , TMEM16A , and CFTR transcript abundance. F : estimate of paracellular conductance ( G p ) obtained from residual G t after inhibition of epithelial Na + channel (ENaC), calcium-activated anion channel (CaCC), and CFTR. For A – D , n = 5 different donors; for E and F , n = 6 different donors. Bars indicate means and SD. Statistical significance between control and TNFα+IL-17-treated epithelia was tested using paired Student’s t test. * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: TNFα+IL-17 increase CFTR activity and expression. After TNFα+IL-17 treatment for 24 h, human airway epithelia were mounted in modified Ussing chambers with symmetric Krebs-Ringer solution gassed with 5% CO 2 . Epithelia were voltage clamped followed by continuous recording of short-circuit current ( I SC ) and transepithelial conductance ( G t ) as pharmacologic agents were sequentially added to the apical chamber. A – D : I SC , Δ I SC , G t , and Δ G t in control and TNFα+IL-17-treated epithelia. E : TNFα+IL-17-induced changes in SCNN1A , TMEM16A , and CFTR transcript abundance. F : estimate of paracellular conductance ( G p ) obtained from residual G t after inhibition of epithelial Na + channel (ENaC), calcium-activated anion channel (CaCC), and CFTR. For A – D , n = 5 different donors; for E and F , n = 6 different donors. Bars indicate means and SD. Statistical significance between control and TNFα+IL-17-treated epithelia was tested using paired Student’s t test. * P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Activity Assay, Expressing, Modification, Inhibition

    TNFα+IL-17 induce apical membrane Cl − / HCO 3 − exchange. Human airway epithelia were treated with either vehicle or TNFα+IL-17 for 48 h. Epithelia were washed, loaded with BCECF, and fluorescence measured with a confocal microscope. A : BCECF-loaded airway epithelia viewed en face. Scale bar, 10 μm. B and C : intracellular pH (pH i ) responses to varying apical buffer composition in control (blue) and TNFα+IL-17-treated (red) epithelia. D : pH i values were converted to [H + ] i and used to calculate net flux (Δ[H + ] i ) in response to removal ( left ) and replenishment ( right ) of Cl − in the apical perfusion buffer ( n = 5 different donors). Bars indicate means ± SD. Groups were compared with paired Student’s t test. ** P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: TNFα+IL-17 induce apical membrane Cl − / HCO 3 − exchange. Human airway epithelia were treated with either vehicle or TNFα+IL-17 for 48 h. Epithelia were washed, loaded with BCECF, and fluorescence measured with a confocal microscope. A : BCECF-loaded airway epithelia viewed en face. Scale bar, 10 μm. B and C : intracellular pH (pH i ) responses to varying apical buffer composition in control (blue) and TNFα+IL-17-treated (red) epithelia. D : pH i values were converted to [H + ] i and used to calculate net flux (Δ[H + ] i ) in response to removal ( left ) and replenishment ( right ) of Cl − in the apical perfusion buffer ( n = 5 different donors). Bars indicate means ± SD. Groups were compared with paired Student’s t test. ** P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques: Fluorescence, Microscopy

    Combination of TNFα and IL-17 increases pH of airway surface liquid (pH ASL ). Primary cultures of differentiated human airway epithelia were treated with TNFα (10 ng/mL), IL-17 (20 ng/mL), or both for the indicated times, and pH ASL was measured using SNARF-1-dextran. A : HCO 3 − /CO 2 -containing Krebs-Ringer ( n = 6). B : TNFα alone in HCO 3 − /CO 2 -containing Krebs-Ringer for indicated times ( n = 6). C : TNFα and IL-17 in HCO 3 − /CO 2 -containing Ringers for indicated times ( n = 5). D : HCO 3 − /CO 2 -free Krebs HEPES buffer ( n = 6). Each data point represents epithelium from a different donor. Light and dark gray circles represent control and cytokine-treated epithelia, respectively. Bars indicate means and SD. * P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: Combination of TNFα and IL-17 increases pH of airway surface liquid (pH ASL ). Primary cultures of differentiated human airway epithelia were treated with TNFα (10 ng/mL), IL-17 (20 ng/mL), or both for the indicated times, and pH ASL was measured using SNARF-1-dextran. A : HCO 3 − /CO 2 -containing Krebs-Ringer ( n = 6). B : TNFα alone in HCO 3 − /CO 2 -containing Krebs-Ringer for indicated times ( n = 6). C : TNFα and IL-17 in HCO 3 − /CO 2 -containing Ringers for indicated times ( n = 5). D : HCO 3 − /CO 2 -free Krebs HEPES buffer ( n = 6). Each data point represents epithelium from a different donor. Light and dark gray circles represent control and cytokine-treated epithelia, respectively. Bars indicate means and SD. * P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques:

    Non-CFTR mechanism(s) mediate TNFα+IL-17-induced airway surface liquid (ASL) alkalinization and operate in tandem with CFTR. Human airway epithelia were treated with TNFα+IL-17 for 24 h, and pH of ASL (pH ASL ) was measured with SNARF-1-dextran in the presence of HCO 3 − /CO 2 . pH ASL values were converted to [H + ] ASL , and net alkalinization was calculated as the difference (Δ[H + ] ASL ) between control and TNFα+IL-17-treated epithelia. A : TNFα+IL-17-induced alkalinization in non-cystic fibrosis (CF) vs. CF epithelia ( n = 12 different donors for non-CF and 11 different donors for CF group). B : TNFα+IL-17-induced alkalinization in CF donors carrying at least one F508-CFTR allele. Epithelia were treated with either vehicle (DMSO) or the recently approved triple combination of CFTR correctors (3 μM VX-445, 18 μM VX-661, 1 μM VX-770) for 48 h, with the addition of cytokines for the last 24 h ( n = 6). CF epithelia in A and B were from different donors and were studied at different times. Bars indicate means ± SD. Groups were compared with unpaired ( A ) or paired ( B ) Student’s t test. ** P

    Journal: American Journal of Physiology - Cell Physiology

    Article Title: TNFα and IL-17 alkalinize airway surface liquid through CFTR and pendrin

    doi: 10.1152/ajpcell.00112.2020

    Figure Lengend Snippet: Non-CFTR mechanism(s) mediate TNFα+IL-17-induced airway surface liquid (ASL) alkalinization and operate in tandem with CFTR. Human airway epithelia were treated with TNFα+IL-17 for 24 h, and pH of ASL (pH ASL ) was measured with SNARF-1-dextran in the presence of HCO 3 − /CO 2 . pH ASL values were converted to [H + ] ASL , and net alkalinization was calculated as the difference (Δ[H + ] ASL ) between control and TNFα+IL-17-treated epithelia. A : TNFα+IL-17-induced alkalinization in non-cystic fibrosis (CF) vs. CF epithelia ( n = 12 different donors for non-CF and 11 different donors for CF group). B : TNFα+IL-17-induced alkalinization in CF donors carrying at least one F508-CFTR allele. Epithelia were treated with either vehicle (DMSO) or the recently approved triple combination of CFTR correctors (3 μM VX-445, 18 μM VX-661, 1 μM VX-770) for 48 h, with the addition of cytokines for the last 24 h ( n = 6). CF epithelia in A and B were from different donors and were studied at different times. Bars indicate means ± SD. Groups were compared with unpaired ( A ) or paired ( B ) Student’s t test. ** P

    Article Snippet: To assess cytokine-induced responses, epithelia were treated on the basolateral side with 10 ng/mL TNFα (R & D Systems), 20 ng/mL IL-17 (R & D Systems), or both for 24 or 48 h based on dose-ranging and time-course studies.

    Techniques:

    Proposed mechanisms of acute kidney injury induced liver dysfunction and systemic inflammation Acute kidney injury causes small intestinal generation of IL-17A and subsequent intestinal injury (villous endothelial apoptosis, epithelial necrosis, increased pro-inflammatory cell translocation and cytokine flux to the liver). These events cause hepatic injury (inflammation, apoptosis and necrosis) with increased generation and release of TNF-α and IL-6 systemically causing further multi-organ injury and systemic inflammation.

    Journal: Laboratory investigation; a journal of technical methods and pathology

    Article Title: Cytokines induce small intestine and liver injury after renal ischemia or nephrectomy

    doi: 10.1038/labinvest.2010.151

    Figure Lengend Snippet: Proposed mechanisms of acute kidney injury induced liver dysfunction and systemic inflammation Acute kidney injury causes small intestinal generation of IL-17A and subsequent intestinal injury (villous endothelial apoptosis, epithelial necrosis, increased pro-inflammatory cell translocation and cytokine flux to the liver). These events cause hepatic injury (inflammation, apoptosis and necrosis) with increased generation and release of TNF-α and IL-6 systemically causing further multi-organ injury and systemic inflammation.

    Article Snippet: Critical roles for TNF-α, IL-6 and IL-17A in generating liver and intestine injury after ischemic or non-ischemic AKI To test the hypothesis that TNF-α, IL-6 and/or IL-17A play key roles in inducing liver and intestine injury after ischemic or non-ischemic AKI, we used complementary approaches using neutralizing antibodies specific for TNF-α, IL-6 and IL-17A (eBiosciences, San Diego, CA) and TNF-α, IL-6, IL-17A and IL-17A receptor (IL-17R) deficient mice (sources described above).

    Techniques: Translocation Assay

    A. Representative gel images (top) and band intensity quantifications (bottom) of semi-quantitative RT-PCR of the pro-inflammatory markers ICAM-1, TNF-α, IL-6, KC, MCP-1 and MIP-2 from ileum of C57BL/6 (WT) mice subjected to sham-operation (Sham) or bilateral nephrectomy (BNx) compared to pro-inflammatory gene expression from the ileum of TNF-α, IL-6 or IL-17A deficient (KO) mice. Tissues were harvested 5 hrs after sham-operation or AKI induction. *P

    Journal: Laboratory investigation; a journal of technical methods and pathology

    Article Title: Cytokines induce small intestine and liver injury after renal ischemia or nephrectomy

    doi: 10.1038/labinvest.2010.151

    Figure Lengend Snippet: A. Representative gel images (top) and band intensity quantifications (bottom) of semi-quantitative RT-PCR of the pro-inflammatory markers ICAM-1, TNF-α, IL-6, KC, MCP-1 and MIP-2 from ileum of C57BL/6 (WT) mice subjected to sham-operation (Sham) or bilateral nephrectomy (BNx) compared to pro-inflammatory gene expression from the ileum of TNF-α, IL-6 or IL-17A deficient (KO) mice. Tissues were harvested 5 hrs after sham-operation or AKI induction. *P

    Article Snippet: Critical roles for TNF-α, IL-6 and IL-17A in generating liver and intestine injury after ischemic or non-ischemic AKI To test the hypothesis that TNF-α, IL-6 and/or IL-17A play key roles in inducing liver and intestine injury after ischemic or non-ischemic AKI, we used complementary approaches using neutralizing antibodies specific for TNF-α, IL-6 and IL-17A (eBiosciences, San Diego, CA) and TNF-α, IL-6, IL-17A and IL-17A receptor (IL-17R) deficient mice (sources described above).

    Techniques: Quantitative RT-PCR, Mouse Assay, Expressing

    Increased hepatic inflammation after ischemic or non-ischemic AKI A. Representative gel images and band intensity quantifications of semi-quantitative RT-PCR of the pro-inflammatory markers ICAM-1, TNF-α, IL-6, IL-17A, KC, MCP-1 and MIP-2 from liver tissues of mice subjected to sham-operation (Sham), bilateral nephrectomy (BNx) or 30 min. renal IR (RIR). Liver tissues were harvested 5 hrs after sham-operation or AKI induction. *P

    Journal: Laboratory investigation; a journal of technical methods and pathology

    Article Title: Cytokines induce small intestine and liver injury after renal ischemia or nephrectomy

    doi: 10.1038/labinvest.2010.151

    Figure Lengend Snippet: Increased hepatic inflammation after ischemic or non-ischemic AKI A. Representative gel images and band intensity quantifications of semi-quantitative RT-PCR of the pro-inflammatory markers ICAM-1, TNF-α, IL-6, IL-17A, KC, MCP-1 and MIP-2 from liver tissues of mice subjected to sham-operation (Sham), bilateral nephrectomy (BNx) or 30 min. renal IR (RIR). Liver tissues were harvested 5 hrs after sham-operation or AKI induction. *P

    Article Snippet: Critical roles for TNF-α, IL-6 and IL-17A in generating liver and intestine injury after ischemic or non-ischemic AKI To test the hypothesis that TNF-α, IL-6 and/or IL-17A play key roles in inducing liver and intestine injury after ischemic or non-ischemic AKI, we used complementary approaches using neutralizing antibodies specific for TNF-α, IL-6 and IL-17A (eBiosciences, San Diego, CA) and TNF-α, IL-6, IL-17A and IL-17A receptor (IL-17R) deficient mice (sources described above).

    Techniques: Quantitative RT-PCR, Mouse Assay

    Increased small intestine necrosis, apoptosis and inflammation after ischemic or non-ischemic AKI A. Representative photomicrographs of ileum from 5 experiments (hematoxylin and eosin staining, magnification 200X and 400X) of mice subjected to sham-operation (Sham), to 30 min. renal ischemia and 5 hrs of reperfusion (RIR) or to bilateral nephrectomy (BNx). Sham operated animals show normal-appearing intestine histology (left panel). As shown in middle upper panel, lower power images (200X) show full thickness of the ileal wall and villi that appear thickened, blunted and inflamed compared to sham. In addition, 5 hours after 30 min. renal IR or bilateral nephrectomy, severe intestine epithelial cell necrosis of villous lining cells and the development of a necrotic epithelial pannus (arrows) over the mucosal surface were observed (middle panel). Finally, we observed prominent capillary endothelial apoptosis within the central villi of ileum (right panel). Enlarged insert shows several apoptotic endothelial cells (red arrow heads) within a villus. B. Representative gel images and band intensity quantifications of semi-quantitative RT-PCR of the pro-inflammatory markers ICAM-1, TNF-α, IL-6, IL-17A, KC, MCP-1 and MIP-2 from ileum of mice subjected to sham-operation (Sham), bilateral nephrectomy (BNx) or 30 min. renal IR (RIR). Tissues were harvested 5 hrs after sham-operation or AKI induction. *P

    Journal: Laboratory investigation; a journal of technical methods and pathology

    Article Title: Cytokines induce small intestine and liver injury after renal ischemia or nephrectomy

    doi: 10.1038/labinvest.2010.151

    Figure Lengend Snippet: Increased small intestine necrosis, apoptosis and inflammation after ischemic or non-ischemic AKI A. Representative photomicrographs of ileum from 5 experiments (hematoxylin and eosin staining, magnification 200X and 400X) of mice subjected to sham-operation (Sham), to 30 min. renal ischemia and 5 hrs of reperfusion (RIR) or to bilateral nephrectomy (BNx). Sham operated animals show normal-appearing intestine histology (left panel). As shown in middle upper panel, lower power images (200X) show full thickness of the ileal wall and villi that appear thickened, blunted and inflamed compared to sham. In addition, 5 hours after 30 min. renal IR or bilateral nephrectomy, severe intestine epithelial cell necrosis of villous lining cells and the development of a necrotic epithelial pannus (arrows) over the mucosal surface were observed (middle panel). Finally, we observed prominent capillary endothelial apoptosis within the central villi of ileum (right panel). Enlarged insert shows several apoptotic endothelial cells (red arrow heads) within a villus. B. Representative gel images and band intensity quantifications of semi-quantitative RT-PCR of the pro-inflammatory markers ICAM-1, TNF-α, IL-6, IL-17A, KC, MCP-1 and MIP-2 from ileum of mice subjected to sham-operation (Sham), bilateral nephrectomy (BNx) or 30 min. renal IR (RIR). Tissues were harvested 5 hrs after sham-operation or AKI induction. *P

    Article Snippet: Critical roles for TNF-α, IL-6 and IL-17A in generating liver and intestine injury after ischemic or non-ischemic AKI To test the hypothesis that TNF-α, IL-6 and/or IL-17A play key roles in inducing liver and intestine injury after ischemic or non-ischemic AKI, we used complementary approaches using neutralizing antibodies specific for TNF-α, IL-6 and IL-17A (eBiosciences, San Diego, CA) and TNF-α, IL-6, IL-17A and IL-17A receptor (IL-17R) deficient mice (sources described above).

    Techniques: Staining, Mouse Assay, Quantitative RT-PCR

    Reduced CD4 + Foxp3 + Treg in L. sigmodontis -infected IL-17A −/− C57BL/6 mice at the site of infection. On day 28 of infection, thoracic ( a , b ) and mLN ( c , d ) cell populations were screened for levels of CD4 + T cells ( a , c ) and CD4 + Foxp3 + Treg ( b , d ) populations. Values are expressed as mean ± SEM and symbols show levels in each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Journal: Parasitology Research

    Article Title: Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ

    doi: 10.1007/s00436-018-5959-7

    Figure Lengend Snippet: Reduced CD4 + Foxp3 + Treg in L. sigmodontis -infected IL-17A −/− C57BL/6 mice at the site of infection. On day 28 of infection, thoracic ( a , b ) and mLN ( c , d ) cell populations were screened for levels of CD4 + T cells ( a , c ) and CD4 + Foxp3 + Treg ( b , d ) populations. Values are expressed as mean ± SEM and symbols show levels in each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Article Snippet: Thereafter, cells were stained with combinations of fluorophores (FITC, PE, PE-Cy7, PerCp-Cy5.5, APC) conjugated with anti-mouse CD4, CD11b, Foxp3, F4/80, GR1, Ly6c, pStat3 (Y705), Rorγt (eBioscience) and IL-17A (Biolegend, San Diego, USA) monoclonal antibodies to determine distinct cell populations.

    Techniques: Infection, Mouse Assay, MANN-WHITNEY

    Impaired functional Th17 cells in L. sigmodontis -infected IL-17A −/− C57BL/6 mice at the site of infection and the draining lymph nodes. On day 28 of infection, thoracic ( a , b ) and mLN ( c , d ) cell populations were screened for levels of CD4 + Rorγt + pStat3 + ( a , c ) and CD4 + Rorγt + pStat3 + IL-17A + Th17 cell ( b , d ) cell populations. Values are expressed as mean ± SEM and symbols show levels in each mouse from one infection experiments ( n = 10 IL-17A −/− and n = 10 WT mice). Statistical significances between the indicated groups were obtained using either the unpaired t test or the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (** p

    Journal: Parasitology Research

    Article Title: Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ

    doi: 10.1007/s00436-018-5959-7

    Figure Lengend Snippet: Impaired functional Th17 cells in L. sigmodontis -infected IL-17A −/− C57BL/6 mice at the site of infection and the draining lymph nodes. On day 28 of infection, thoracic ( a , b ) and mLN ( c , d ) cell populations were screened for levels of CD4 + Rorγt + pStat3 + ( a , c ) and CD4 + Rorγt + pStat3 + IL-17A + Th17 cell ( b , d ) cell populations. Values are expressed as mean ± SEM and symbols show levels in each mouse from one infection experiments ( n = 10 IL-17A −/− and n = 10 WT mice). Statistical significances between the indicated groups were obtained using either the unpaired t test or the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (** p

    Article Snippet: Thereafter, cells were stained with combinations of fluorophores (FITC, PE, PE-Cy7, PerCp-Cy5.5, APC) conjugated with anti-mouse CD4, CD11b, Foxp3, F4/80, GR1, Ly6c, pStat3 (Y705), Rorγt (eBioscience) and IL-17A (Biolegend, San Diego, USA) monoclonal antibodies to determine distinct cell populations.

    Techniques: Functional Assay, Infection, Mouse Assay, MANN-WHITNEY

    Reduced worm burden in L. sigmodontis -infected IL-17A −/− C57BL/6 mice. Groups of WT and IL-17A −/− C57BL/6 mice were infected with L. sigmodontis for 28 days (d28). Thereafter, absolute worm burden ( a ), life stage ( b ) and adult worm length ( c ) were determined in individual mice. Values are expressed as mean ± SEM from four independent infection experiments ( n = 20 IL-17A −/− and n = 23 WT mice). Data in c show mean ± SEM of adult worm length per mouse from the total n = 53 female and n = 38 male adult worms isolated from IL-17A −/− mice and n = 70 female and n = 107 male adult worms isolated from WT mice. Values in d show absolute worm burden as mean ± SEM from groups of WT ( n = 10) and IL-17A −/− C57BL/6 mice ( n = 10) on day 7 p.i. (d7). Statistical significances between the indicated groups were obtained using Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Journal: Parasitology Research

    Article Title: Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ

    doi: 10.1007/s00436-018-5959-7

    Figure Lengend Snippet: Reduced worm burden in L. sigmodontis -infected IL-17A −/− C57BL/6 mice. Groups of WT and IL-17A −/− C57BL/6 mice were infected with L. sigmodontis for 28 days (d28). Thereafter, absolute worm burden ( a ), life stage ( b ) and adult worm length ( c ) were determined in individual mice. Values are expressed as mean ± SEM from four independent infection experiments ( n = 20 IL-17A −/− and n = 23 WT mice). Data in c show mean ± SEM of adult worm length per mouse from the total n = 53 female and n = 38 male adult worms isolated from IL-17A −/− mice and n = 70 female and n = 107 male adult worms isolated from WT mice. Values in d show absolute worm burden as mean ± SEM from groups of WT ( n = 10) and IL-17A −/− C57BL/6 mice ( n = 10) on day 7 p.i. (d7). Statistical significances between the indicated groups were obtained using Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Article Snippet: Thereafter, cells were stained with combinations of fluorophores (FITC, PE, PE-Cy7, PerCp-Cy5.5, APC) conjugated with anti-mouse CD4, CD11b, Foxp3, F4/80, GR1, Ly6c, pStat3 (Y705), Rorγt (eBioscience) and IL-17A (Biolegend, San Diego, USA) monoclonal antibodies to determine distinct cell populations.

    Techniques: Infection, Mouse Assay, Isolation, MANN-WHITNEY

    Flow cytometry-based differentiation of TC cells revealed comparable monocyte, macrophage, neutrophil and eosinophil numbers. Groups of WT and IL-17A −/− C57BL/6 mice were infected with L. sigmodontis for 28 days. Within the TC, the site of infection, the absolute number of CD11b + SiglecF − Ly6c + monocytes ( a ), CD11b + SiglecF − F4/80 + macrophages ( b ), CD11b + SiglecF − GR1 + neutrophils ( c ) and CD11b + SiglecF + eosinophils ( d ) was determined in individual mice using flow cytometry. Values are expressed as mean ± SEM and symbols show levels in each mouse from one infection experiments ( n = 10 IL-17A −/− and n = 10 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests

    Journal: Parasitology Research

    Article Title: Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ

    doi: 10.1007/s00436-018-5959-7

    Figure Lengend Snippet: Flow cytometry-based differentiation of TC cells revealed comparable monocyte, macrophage, neutrophil and eosinophil numbers. Groups of WT and IL-17A −/− C57BL/6 mice were infected with L. sigmodontis for 28 days. Within the TC, the site of infection, the absolute number of CD11b + SiglecF − Ly6c + monocytes ( a ), CD11b + SiglecF − F4/80 + macrophages ( b ), CD11b + SiglecF − GR1 + neutrophils ( c ) and CD11b + SiglecF + eosinophils ( d ) was determined in individual mice using flow cytometry. Values are expressed as mean ± SEM and symbols show levels in each mouse from one infection experiments ( n = 10 IL-17A −/− and n = 10 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests

    Article Snippet: Thereafter, cells were stained with combinations of fluorophores (FITC, PE, PE-Cy7, PerCp-Cy5.5, APC) conjugated with anti-mouse CD4, CD11b, Foxp3, F4/80, GR1, Ly6c, pStat3 (Y705), Rorγt (eBioscience) and IL-17A (Biolegend, San Diego, USA) monoclonal antibodies to determine distinct cell populations.

    Techniques: Flow Cytometry, Cytometry, Mouse Assay, Infection, MANN-WHITNEY

    Infected IL-17A −/− mice show dominant filarial-specific IFN-γ responses. On day 28 p.i., draining mLN cells (5 × 10 5 cells/well) from individual mice were plated in RPMI 1640 medium with supplements and left either alone (Cont.) or stimulated with LsAg (50 μg/ml) or αCD3/αCD28 (5/1.25 μg/ml) in triplicates. After 72 h, the culture supernatant was removed and screened for the presence of IFN-γ ( a ), IL-4 ( b ), IL-6 ( c ) and IL-21 ( d ) by ELISA. Graphs show cytokine responses and values are expressed as mean ± SEM from each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Journal: Parasitology Research

    Article Title: Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ

    doi: 10.1007/s00436-018-5959-7

    Figure Lengend Snippet: Infected IL-17A −/− mice show dominant filarial-specific IFN-γ responses. On day 28 p.i., draining mLN cells (5 × 10 5 cells/well) from individual mice were plated in RPMI 1640 medium with supplements and left either alone (Cont.) or stimulated with LsAg (50 μg/ml) or αCD3/αCD28 (5/1.25 μg/ml) in triplicates. After 72 h, the culture supernatant was removed and screened for the presence of IFN-γ ( a ), IL-4 ( b ), IL-6 ( c ) and IL-21 ( d ) by ELISA. Graphs show cytokine responses and values are expressed as mean ± SEM from each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Article Snippet: Thereafter, cells were stained with combinations of fluorophores (FITC, PE, PE-Cy7, PerCp-Cy5.5, APC) conjugated with anti-mouse CD4, CD11b, Foxp3, F4/80, GR1, Ly6c, pStat3 (Y705), Rorγt (eBioscience) and IL-17A (Biolegend, San Diego, USA) monoclonal antibodies to determine distinct cell populations.

    Techniques: Infection, Mouse Assay, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    Reduced eotaxin-1 and CCL17 levels in L. sigmodontis -infected IL-17A −/− C57BL/6 mice. Groups of WT and IL-17A −/− C57BL/6 mice were infected with L. sigmodontis for 28 days. Levels of IL-6 ( a ), IL-21 ( b ), RANTES ( c ), eotaxin ( d ), granzyme B ( e ) and CCL17 ( f ) were determined in the lavage fluid from the TC by ELISA. Values are expressed as mean ± SEM and symbols show levels in each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Journal: Parasitology Research

    Article Title: Absence of IL-17A in Litomosoides sigmodontis-infected mice influences worm development and drives elevated filarial-specific IFN-γ

    doi: 10.1007/s00436-018-5959-7

    Figure Lengend Snippet: Reduced eotaxin-1 and CCL17 levels in L. sigmodontis -infected IL-17A −/− C57BL/6 mice. Groups of WT and IL-17A −/− C57BL/6 mice were infected with L. sigmodontis for 28 days. Levels of IL-6 ( a ), IL-21 ( b ), RANTES ( c ), eotaxin ( d ), granzyme B ( e ) and CCL17 ( f ) were determined in the lavage fluid from the TC by ELISA. Values are expressed as mean ± SEM and symbols show levels in each mouse from three independent infection experiments ( n = 10 IL-17A −/− and n = 13 WT mice). Statistical significances between the indicated groups were obtained using the Mann-Whitney U tests. Asterisks denote significant differences between the groups indicated by the brackets (* p

    Article Snippet: Thereafter, cells were stained with combinations of fluorophores (FITC, PE, PE-Cy7, PerCp-Cy5.5, APC) conjugated with anti-mouse CD4, CD11b, Foxp3, F4/80, GR1, Ly6c, pStat3 (Y705), Rorγt (eBioscience) and IL-17A (Biolegend, San Diego, USA) monoclonal antibodies to determine distinct cell populations.

    Techniques: Infection, Mouse Assay, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

    Reduction of the lesion size in the lungs of IL‐17A KO mice after M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. The mice were sacrificed 30, 60, and 120 days after infection, and formalin‐fixed sections were stained with hematoxylin and eosin. Representative lung tissue specimens from the wild‐type C57BL/6 mice (left panel) and the IL‐17A KO mice (right panel) are shown. Magnification, ×40 (A), ×400 (B).

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: Reduction of the lesion size in the lungs of IL‐17A KO mice after M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. The mice were sacrificed 30, 60, and 120 days after infection, and formalin‐fixed sections were stained with hematoxylin and eosin. Representative lung tissue specimens from the wild‐type C57BL/6 mice (left panel) and the IL‐17A KO mice (right panel) are shown. Magnification, ×40 (A), ×400 (B).

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Mouse Assay, Infection, Staining

    Th1‐type cytokine expression in the lungs of the surviving IL‐17A KO mice after pulmonary M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. The expression levels of IFN‐γ and TNF expression in the infected lungs were analyzed on day 250 after M. tuberculosis H37Rv infection by real‐time RT‐PCR (A), and production of IFN‐γ and TNF in the infected lungs was analyzed by the CBA system (B). The statistical analysis was performed with Student's t ‐test. Asterisks (*) indicate significant difference between two groups.

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: Th1‐type cytokine expression in the lungs of the surviving IL‐17A KO mice after pulmonary M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. The expression levels of IFN‐γ and TNF expression in the infected lungs were analyzed on day 250 after M. tuberculosis H37Rv infection by real‐time RT‐PCR (A), and production of IFN‐γ and TNF in the infected lungs was analyzed by the CBA system (B). The statistical analysis was performed with Student's t ‐test. Asterisks (*) indicate significant difference between two groups.

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Expressing, Mouse Assay, Infection, Quantitative RT-PCR, Crocin Bleaching Assay

    TCR γδ + T cells were the major IL‐17A‐producing cells in the lungs of M. tuberculosis ‐infected mice. Wild‐type C57BL/6 mice were inoculated i.t. with M. tuberculosis H37Rv or left untreated (A and B). The PIF cells (5 × 10 5 cells) were prepared on day 60, and were cultured with PPD (5 μg/ml) in the presence of naive spleen antigen‐presenting cells (1 × 10 5 cells) for 18 h at 37°C, and with GolgiPlug for the last 6 h. The cells were also stimulated with PMA and ionomycin. After the culture, the cells were surface stained with FITC‐CD3e, PerCP‐Cy5.5, or APC‐conjugated anti‐TCR Cβ and APC‐conjugated TCR Cδ mAbs. Surface‐stained cells were subjected to intercellular cytokine staining with a PE‐conjugated anti‐IL‐17A mAb. The samples were analyzed by FCM (A, naïve; B, infected). Wild‐type C57BL/6, IL‐17A KO, and TCR Cδ KO mice were inoculated i.t. with 1 × 10 3 CFU of M. tuberculosis H37Rv (C), and the CFU in the lungs was determined on day 60 after the infection. The statistical analysis was performed with ANOVA. Asterisks (*) indicate significant difference between two groups.

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: TCR γδ + T cells were the major IL‐17A‐producing cells in the lungs of M. tuberculosis ‐infected mice. Wild‐type C57BL/6 mice were inoculated i.t. with M. tuberculosis H37Rv or left untreated (A and B). The PIF cells (5 × 10 5 cells) were prepared on day 60, and were cultured with PPD (5 μg/ml) in the presence of naive spleen antigen‐presenting cells (1 × 10 5 cells) for 18 h at 37°C, and with GolgiPlug for the last 6 h. The cells were also stimulated with PMA and ionomycin. After the culture, the cells were surface stained with FITC‐CD3e, PerCP‐Cy5.5, or APC‐conjugated anti‐TCR Cβ and APC‐conjugated TCR Cδ mAbs. Surface‐stained cells were subjected to intercellular cytokine staining with a PE‐conjugated anti‐IL‐17A mAb. The samples were analyzed by FCM (A, naïve; B, infected). Wild‐type C57BL/6, IL‐17A KO, and TCR Cδ KO mice were inoculated i.t. with 1 × 10 3 CFU of M. tuberculosis H37Rv (C), and the CFU in the lungs was determined on day 60 after the infection. The statistical analysis was performed with ANOVA. Asterisks (*) indicate significant difference between two groups.

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Infection, Mouse Assay, Cell Culture, Staining

    BCG vaccination did not induce Th17 cells in the lungs after M. tuberculosis challenge. Wild‐type C57BL/6 mice were vaccinated with M. bovis BCG 30 or 60 days before M. tuberculosis H37Rv infection. The PIF cells (5 × 10 5 cells) were prepared on the 4th week after the M. tuberculosis infection, and were cultured with PPD (5 μg/ml) in the presence of naive spleen antigen presenting cells (1 × 10 5 cells) for 18 h at 37°C, and with GolgiPlug for the last 6 h. After the culture, the cells were surface stained with FITC‐CD3 and APC‐conjugated anti‐CD4. Surface‐stained cells were subjected to intercellular cytokine staining with a PE‐conjugated anti‐IL‐17A mAb. The samples were analyzed by FCM.

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: BCG vaccination did not induce Th17 cells in the lungs after M. tuberculosis challenge. Wild‐type C57BL/6 mice were vaccinated with M. bovis BCG 30 or 60 days before M. tuberculosis H37Rv infection. The PIF cells (5 × 10 5 cells) were prepared on the 4th week after the M. tuberculosis infection, and were cultured with PPD (5 μg/ml) in the presence of naive spleen antigen presenting cells (1 × 10 5 cells) for 18 h at 37°C, and with GolgiPlug for the last 6 h. After the culture, the cells were surface stained with FITC‐CD3 and APC‐conjugated anti‐CD4. Surface‐stained cells were subjected to intercellular cytokine staining with a PE‐conjugated anti‐IL‐17A mAb. The samples were analyzed by FCM.

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Mouse Assay, Infection, Cell Culture, Staining

    The survival of IL‐17A KO mice after mycobacterial infection. Groups of 11–13 mice were infected i.t. with 1 × 10 5 (A) or 1 × 10 3 (B) CFU of M. tuberculosis H37Rv, and the survival rates were monitored. The statistical significance of the differences in survival was determined by the generalized Wilcoxon's test. P = 0.0018 (A) and P = 0.0052 (B), respectively. The asterisk (*) indicates that the difference was considered to be significant.

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: The survival of IL‐17A KO mice after mycobacterial infection. Groups of 11–13 mice were infected i.t. with 1 × 10 5 (A) or 1 × 10 3 (B) CFU of M. tuberculosis H37Rv, and the survival rates were monitored. The statistical significance of the differences in survival was determined by the generalized Wilcoxon's test. P = 0.0018 (A) and P = 0.0052 (B), respectively. The asterisk (*) indicates that the difference was considered to be significant.

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Mouse Assay, Infection

    The Th1 immune response in the early phase against M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. Mice were sacrificed 30, 60, and 90 days after infection, and the lung lymphocytes were stimulated with PPD, and the percentages of IFN‐γ producing CD4 + cells in the CD3 + T cell population were determined using FCM (A). In some experiments, the concentrations of IFN‐γ in the supernatants of the lung lymphocytes were determined by an ELISA using the DuoSet ELISA development kit, according to the manufacturer's protocol (B). The statistical analysis was performed with Student's t ‐test. Asterisks (*) indicate significant difference between two groups.

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: The Th1 immune response in the early phase against M. tuberculosis infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with M. tuberculosis H37Rv. Mice were sacrificed 30, 60, and 90 days after infection, and the lung lymphocytes were stimulated with PPD, and the percentages of IFN‐γ producing CD4 + cells in the CD3 + T cell population were determined using FCM (A). In some experiments, the concentrations of IFN‐γ in the supernatants of the lung lymphocytes were determined by an ELISA using the DuoSet ELISA development kit, according to the manufacturer's protocol (B). The statistical analysis was performed with Student's t ‐test. Asterisks (*) indicate significant difference between two groups.

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Infection, Mouse Assay, Enzyme-linked Immunosorbent Assay

    The bacterial growth in various organs of IL‐17A KO mice after mycobacterial infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with 1 × 10 3 CFU of M. tuberculosis H37Rv, and the CFU in the lungs (A), livers (B), and spleens (C) was determined on days 30, 60, and 120 after the infection. The statistical analysis was performed with Student's t ‐test. The asterisk (*) indicates that there was a significant difference compared with wild‐type C57BL/6 mice.

    Journal: Immunity, Inflammation and Disease

    Article Title: Involvement of IL‐17A‐producing TCR γδ T cells in late protective immunity against pulmonary Mycobacterium tuberculosis infection

    doi: 10.1002/iid3.121

    Figure Lengend Snippet: The bacterial growth in various organs of IL‐17A KO mice after mycobacterial infection. Wild‐type C57BL/6 or IL‐17A KO mice were inoculated i.t. with 1 × 10 3 CFU of M. tuberculosis H37Rv, and the CFU in the lungs (A), livers (B), and spleens (C) was determined on days 30, 60, and 120 after the infection. The statistical analysis was performed with Student's t ‐test. The asterisk (*) indicates that there was a significant difference compared with wild‐type C57BL/6 mice.

    Article Snippet: For both intracellular IL‐17A and IFN‐γ staining, cells were detected by a FACSCalibur flow cytometer (BD).

    Techniques: Mouse Assay, Infection