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normal human lung fibroblasts mrc 5  (ATCC)


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    ATCC normal human lung fibroblasts mrc 5
    Normal Human Lung Fibroblasts Mrc 5, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 5423 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+lung+fibroblasts/MRC-5/pm42280248-149-17-22
    Average 99 stars, based on 5423 article reviews
    normal human lung fibroblasts mrc 5 - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    Suspension:

    Article Title: A 3D Organotypic Human Bronchial Model Reveals Persistent Infection and Modulated Inflammatory Response when Exposed to Brucella abortus
    Article Snippet: Briefly, the inner compartment of Transwell inserts (0.33 μm pore size; Costar, Corning Inc., Corning, NY, USA) was incubated for 30 min at 37 °C with a solution of collagen type I (Gibco, Thermo Fisher Scientific, Waltham, MA, USA, 1.1 mg/mL in MEM medium) to allow collagen coating. .. A suspension of human lung fibroblasts (MRC-5 cell line; ATCC, Manassas, VA, USA) was added at 2 × 10 4 cells/Transwell in MEM containing 10% FCS and 1.1 mg/mL type I collagen and incubated for 2 h at 37 °C. ..

    Incubation:

    Article Title: A 3D Organotypic Human Bronchial Model Reveals Persistent Infection and Modulated Inflammatory Response when Exposed to Brucella abortus
    Article Snippet: Briefly, the inner compartment of Transwell inserts (0.33 μm pore size; Costar, Corning Inc., Corning, NY, USA) was incubated for 30 min at 37 °C with a solution of collagen type I (Gibco, Thermo Fisher Scientific, Waltham, MA, USA, 1.1 mg/mL in MEM medium) to allow collagen coating. .. A suspension of human lung fibroblasts (MRC-5 cell line; ATCC, Manassas, VA, USA) was added at 2 × 10 4 cells/Transwell in MEM containing 10% FCS and 1.1 mg/mL type I collagen and incubated for 2 h at 37 °C. ..

    Cell Culture:

    Article Title: Extracellular ATP drives tryptophan metabolism and aryl hydrocarbon receptor activation to promote cellular senescence.
    Article Snippet: Epacadostat, a selective IDO1 inhibitor (94, 95), was from Selleck Chemicals LLC (Houston, TX). .. WI-38 and IMR-90 human lung fibroblasts were purchased from American Type Culture Collection (ATCC; Manassas, VA) and cultured in Eagle’s Minimal Essential Medium (EMEM) supplemented with 2 mM glutamine, 100 U/ml penicillin, 100 μg/ml streptomycin and 10% fetal bovine serum. .. For Trp-depletion experiments, WI-38 cells were cultured in Trpfree DMEM (US Biologicals; Salem, MA) supplemented with 2 mM glutamine, 100 U/ml penicillin, 100 μg/ml streptomycin and dialyzed FBS (Thermo Fisher Scientific Inc; Waltham, MA).

    Article Title: Anti-fibrotic compositions comprising FENDRR or fragments or variants thereof and methods of production and use thereof
    Article Snippet: The RNA concentration and quality were determined with a NanoDrop ND-1000 Spectrophotometer (NanoDrop Tech., Rockland, DE) with an A260/A280 ratio>1.8 and an A260/A230 ratio>1.7. .. Cell culture: HEK 293T cells and human lung fibroblasts (HFL1, CCD-8Lu, and LL29) were purchased from the American Type Culture Collection (ATCC) (Manassas, VA, USA). .. HEK 293A cells were purchased from Invitrogen.

    Article Title: Anti-EDB antibodies and antibody-drug conjugates
    Article Snippet: .. In Vitro Cytotoxicity of EDB ADCs Cell Culture WI38-VA13 are SV40-transformed human lung fibroblasts obtained from ATCC and maintained in MEM Eagles media (Cell-Gro), supplemented with 10% FBS, 1% MEM non-essential amino acids, 1% sodium pyruvate, 100 units/ml penicillin-streptomycin, and 2 mM GLUTAMAX® (Gibco; glutamine substitute). .. HT29 are derived from human colorectal carcinoma (ATCC) and maintained in DMEM media supplemented with 10% FBS and 1% glutamine.

    In Vitro:

    Article Title: Anti-EDB antibodies and antibody-drug conjugates
    Article Snippet: .. In Vitro Cytotoxicity of EDB ADCs Cell Culture WI38-VA13 are SV40-transformed human lung fibroblasts obtained from ATCC and maintained in MEM Eagles media (Cell-Gro), supplemented with 10% FBS, 1% MEM non-essential amino acids, 1% sodium pyruvate, 100 units/ml penicillin-streptomycin, and 2 mM GLUTAMAX® (Gibco; glutamine substitute). .. HT29 are derived from human colorectal carcinoma (ATCC) and maintained in DMEM media supplemented with 10% FBS and 1% glutamine.

    other:

    Article Title: Spatio-temporal dynamics of Hendra virus in Australia reveal stable maintenance of diverse viral clades among Pteropus bats
    Article Snippet: Human lung fibroblasts (HFL-1, ATCC CCL-153), black flying fox kidney cells (PaKiT, (1)), horse dermal fibroblasts (NBL-6, ATCC CCL-57), Vero E6 and Vero CCL-81 cells were used in this study.



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    GM-CSF-induced CD14 + CD16 + monocyte-derived macrophages promoted fibrotic activation of lung <t>fibroblasts,</t> an effect depends upon TREM2 expression. (A) Volcano plot showing DEG in fibroblasts from SScLO compared to those from HCs ( GSE128169 ). Fibrotic activation genes, including POSTN , COL1A1 , COL3A1 , COL4A1 , COL5A1 , COL8A1 , TGFBI , and ACTA2 , were significantly upregulated in SScLO fibroblasts. (B) Schematic diagram of the co-culture experimental design. Monocytes (CD14 + CD16 - or CD14 + CD16 + ) were differentiated into macrophages using GM-CSF for 7 days, then co-cultured with human lung fibroblasts for 5 days with or without TREM2 inhibitor. Bulk RNA sequencing and western blot analyses were performed to assess gene expression and protein levels, respectively. (C) Volcano plots showing DEG in fibroblasts co-cultured with CD14 + CD16 - vs. CD14 + CD16 + macrophages (left) and CD14 + CD16 + macrophages with or without TREM2 inhibitor (right). All macrophages were derived from SSc-ILD patients. Co-culture with CD14 + CD16 + macrophages induced fibrotic gene expression ( POSTN , COL7A1 , ACTA2 , and TGFBI ), which was significantly reduced by TREM2 inhibition. Upregulated genes are shown in red (FC > 2, adj. p < 0.05), downregulated in blue (FC < -2, adj. p < 0.05), and non-significant genes in black. Dotted lines indicate statistical thresholds. (D) Representative western blot images of COL7A1 (34 kDa), COL3A1 (200 kDa), COL1A1 (220 kDa), and α-SMA (42 kDa); GAPDH (37 kDa) was used as a loading control. Conditions with TREM2 inhibitor are indicated in red. (E–H) Quantification of protein levels normalized to GAPDH: (E) COL7A1, (F) COL3A1, (G) COL1A1, and (H) α-SMA. Expression of COL7A1, COL1A1, and α-SMA was significantly elevated in fibroblasts co-cultured with CD14 + CD16 + monocytes derived macrophages from SSc-ILD compared to HCs and CD14 + CD16 - monocytes derived macrophages from SSc-ILD. COL3A1 expression was also elevated in SSc-ILD fibroblasts compared to HCs. TREM2 inhibition markedly reduced expression of all fibrotic markers. Statistical analysis was conducted using MANOVA, followed by Tukey’s post-hoc multiple comparisons test. Data are presented as mean ± SEM, with n = 6 per group. Statistical significance is indicated as * p < 0.05, ** p < 0.01 for comparisons between SSc-ILD and HCs within the same subset; # p < 0.05, ## p < 0.01 for comparisons between CD14 + CD16 - and CD14 + CD16 + subsets within SSc-ILD patients; $ p < 0.05, $$ p < 0.01 for comparisons between SSc-ILD and TREM2 inhibitor within the same subset.
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    A) Hydrogels were composed of either 0% or 50% mixture of tyramine-modified silk and were exposed to media without or with 5 ng/mL TGFβ. After hydrogels were cast, 25,000 <t>NHLF</t> cells were seeded on the surface. B) SEM imaging of the surface of the silk hydrogels incubated without cells for Day 0 and Day 14. C) Live/Dead imaging of Calcein AM for live cells (green) and Ethidium Homodimer-1 for dead cells (red) indicated cytocompatibility. D) Alamar Blue Assay for metabolic activity indicated that 0% gels showed an increase in activity over 14 days, while 50% gels plateaued from day 7 to 14. E) Mammalian β-Galactosidase Assay for senescence revealed no change for any timepoints tested over 14 days. N=3-4, Error bars = SEM.TCP = Tissue Culture Plate, T-= without TGFβ, T+ = 5 ng/mL of TGFβ. Two-way ANOVA, Tukey’s: ns = not significant p > 0.05, * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001.
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    imr90 human lung fibroblasts  (ATCC)
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    A) Hydrogels were composed of either 0% or 50% mixture of tyramine-modified silk and were exposed to media without or with 5 ng/mL TGFβ. After hydrogels were cast, 25,000 <t>NHLF</t> cells were seeded on the surface. B) SEM imaging of the surface of the silk hydrogels incubated without cells for Day 0 and Day 14. C) Live/Dead imaging of Calcein AM for live cells (green) and Ethidium Homodimer-1 for dead cells (red) indicated cytocompatibility. D) Alamar Blue Assay for metabolic activity indicated that 0% gels showed an increase in activity over 14 days, while 50% gels plateaued from day 7 to 14. E) Mammalian β-Galactosidase Assay for senescence revealed no change for any timepoints tested over 14 days. N=3-4, Error bars = SEM.TCP = Tissue Culture Plate, T-= without TGFβ, T+ = 5 ng/mL of TGFβ. Two-way ANOVA, Tukey’s: ns = not significant p > 0.05, * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001.
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    lentiviral particles human lung fibroblasts cell lines imr 90  (ATCC)
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    ATCC lentiviral particles human lung fibroblasts cell lines imr 90
    A) Hydrogels were composed of either 0% or 50% mixture of tyramine-modified silk and were exposed to media without or with 5 ng/mL TGFβ. After hydrogels were cast, 25,000 <t>NHLF</t> cells were seeded on the surface. B) SEM imaging of the surface of the silk hydrogels incubated without cells for Day 0 and Day 14. C) Live/Dead imaging of Calcein AM for live cells (green) and Ethidium Homodimer-1 for dead cells (red) indicated cytocompatibility. D) Alamar Blue Assay for metabolic activity indicated that 0% gels showed an increase in activity over 14 days, while 50% gels plateaued from day 7 to 14. E) Mammalian β-Galactosidase Assay for senescence revealed no change for any timepoints tested over 14 days. N=3-4, Error bars = SEM.TCP = Tissue Culture Plate, T-= without TGFβ, T+ = 5 ng/mL of TGFβ. Two-way ANOVA, Tukey’s: ns = not significant p > 0.05, * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001.
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    Image Search Results


    GM-CSF-induced CD14 + CD16 + monocyte-derived macrophages promoted fibrotic activation of lung fibroblasts, an effect depends upon TREM2 expression. (A) Volcano plot showing DEG in fibroblasts from SScLO compared to those from HCs ( GSE128169 ). Fibrotic activation genes, including POSTN , COL1A1 , COL3A1 , COL4A1 , COL5A1 , COL8A1 , TGFBI , and ACTA2 , were significantly upregulated in SScLO fibroblasts. (B) Schematic diagram of the co-culture experimental design. Monocytes (CD14 + CD16 - or CD14 + CD16 + ) were differentiated into macrophages using GM-CSF for 7 days, then co-cultured with human lung fibroblasts for 5 days with or without TREM2 inhibitor. Bulk RNA sequencing and western blot analyses were performed to assess gene expression and protein levels, respectively. (C) Volcano plots showing DEG in fibroblasts co-cultured with CD14 + CD16 - vs. CD14 + CD16 + macrophages (left) and CD14 + CD16 + macrophages with or without TREM2 inhibitor (right). All macrophages were derived from SSc-ILD patients. Co-culture with CD14 + CD16 + macrophages induced fibrotic gene expression ( POSTN , COL7A1 , ACTA2 , and TGFBI ), which was significantly reduced by TREM2 inhibition. Upregulated genes are shown in red (FC > 2, adj. p < 0.05), downregulated in blue (FC < -2, adj. p < 0.05), and non-significant genes in black. Dotted lines indicate statistical thresholds. (D) Representative western blot images of COL7A1 (34 kDa), COL3A1 (200 kDa), COL1A1 (220 kDa), and α-SMA (42 kDa); GAPDH (37 kDa) was used as a loading control. Conditions with TREM2 inhibitor are indicated in red. (E–H) Quantification of protein levels normalized to GAPDH: (E) COL7A1, (F) COL3A1, (G) COL1A1, and (H) α-SMA. Expression of COL7A1, COL1A1, and α-SMA was significantly elevated in fibroblasts co-cultured with CD14 + CD16 + monocytes derived macrophages from SSc-ILD compared to HCs and CD14 + CD16 - monocytes derived macrophages from SSc-ILD. COL3A1 expression was also elevated in SSc-ILD fibroblasts compared to HCs. TREM2 inhibition markedly reduced expression of all fibrotic markers. Statistical analysis was conducted using MANOVA, followed by Tukey’s post-hoc multiple comparisons test. Data are presented as mean ± SEM, with n = 6 per group. Statistical significance is indicated as * p < 0.05, ** p < 0.01 for comparisons between SSc-ILD and HCs within the same subset; # p < 0.05, ## p < 0.01 for comparisons between CD14 + CD16 - and CD14 + CD16 + subsets within SSc-ILD patients; $ p < 0.05, $$ p < 0.01 for comparisons between SSc-ILD and TREM2 inhibitor within the same subset.

    Journal: Frontiers in Immunology

    Article Title: CD14 + CD16 + monocyte-derived TREM2 macrophages promote lung fibrosis in systemic sclerosis–interstitial lung disease

    doi: 10.3389/fimmu.2026.1748574

    Figure Lengend Snippet: GM-CSF-induced CD14 + CD16 + monocyte-derived macrophages promoted fibrotic activation of lung fibroblasts, an effect depends upon TREM2 expression. (A) Volcano plot showing DEG in fibroblasts from SScLO compared to those from HCs ( GSE128169 ). Fibrotic activation genes, including POSTN , COL1A1 , COL3A1 , COL4A1 , COL5A1 , COL8A1 , TGFBI , and ACTA2 , were significantly upregulated in SScLO fibroblasts. (B) Schematic diagram of the co-culture experimental design. Monocytes (CD14 + CD16 - or CD14 + CD16 + ) were differentiated into macrophages using GM-CSF for 7 days, then co-cultured with human lung fibroblasts for 5 days with or without TREM2 inhibitor. Bulk RNA sequencing and western blot analyses were performed to assess gene expression and protein levels, respectively. (C) Volcano plots showing DEG in fibroblasts co-cultured with CD14 + CD16 - vs. CD14 + CD16 + macrophages (left) and CD14 + CD16 + macrophages with or without TREM2 inhibitor (right). All macrophages were derived from SSc-ILD patients. Co-culture with CD14 + CD16 + macrophages induced fibrotic gene expression ( POSTN , COL7A1 , ACTA2 , and TGFBI ), which was significantly reduced by TREM2 inhibition. Upregulated genes are shown in red (FC > 2, adj. p < 0.05), downregulated in blue (FC < -2, adj. p < 0.05), and non-significant genes in black. Dotted lines indicate statistical thresholds. (D) Representative western blot images of COL7A1 (34 kDa), COL3A1 (200 kDa), COL1A1 (220 kDa), and α-SMA (42 kDa); GAPDH (37 kDa) was used as a loading control. Conditions with TREM2 inhibitor are indicated in red. (E–H) Quantification of protein levels normalized to GAPDH: (E) COL7A1, (F) COL3A1, (G) COL1A1, and (H) α-SMA. Expression of COL7A1, COL1A1, and α-SMA was significantly elevated in fibroblasts co-cultured with CD14 + CD16 + monocytes derived macrophages from SSc-ILD compared to HCs and CD14 + CD16 - monocytes derived macrophages from SSc-ILD. COL3A1 expression was also elevated in SSc-ILD fibroblasts compared to HCs. TREM2 inhibition markedly reduced expression of all fibrotic markers. Statistical analysis was conducted using MANOVA, followed by Tukey’s post-hoc multiple comparisons test. Data are presented as mean ± SEM, with n = 6 per group. Statistical significance is indicated as * p < 0.05, ** p < 0.01 for comparisons between SSc-ILD and HCs within the same subset; # p < 0.05, ## p < 0.01 for comparisons between CD14 + CD16 - and CD14 + CD16 + subsets within SSc-ILD patients; $ p < 0.05, $$ p < 0.01 for comparisons between SSc-ILD and TREM2 inhibitor within the same subset.

    Article Snippet: Macrophages differentiated from monocyte subsets by GM-CSF from SSc-ILD patients were cultured for 7 days and subsequently co-cultured with commercially sourced human lung fibroblasts (ACBR 469, Cell Systems, Kirkland, WA, USA) for 5 days, with or without treatment with a TREM2 inhibitor (BLP-NR018, Alomone Labs, Jerusalem, Israel).

    Techniques: Derivative Assay, Activation Assay, Expressing, Co-Culture Assay, Cell Culture, RNA Sequencing, Western Blot, Gene Expression, Inhibition, Control

    TREM2 macrophages and fibrotic progression in SSc-ILD. This schematic illustrates the proposed mechanism by which GM-CSF–induced monocyte-derived macrophages differentiate and promote lung fibrosis in patients with SSc-ILD. In SSc-ILD, recruited monocytes stimulated by GM-CSF upregulate TREM2 and GPNMB , leading to increased secretion of cytokines such as CCL2 and TGF-β1. CCL2 promotes additional recruitment of monocytes via the CCL2-CCR2 axis. These TREM2 + macrophages enhance fibroblast activation through TGF-β1 production, driving fibroblast to myofibroblast differentiation and contributing to fibrotic remodeling in the lung.

    Journal: Frontiers in Immunology

    Article Title: CD14 + CD16 + monocyte-derived TREM2 macrophages promote lung fibrosis in systemic sclerosis–interstitial lung disease

    doi: 10.3389/fimmu.2026.1748574

    Figure Lengend Snippet: TREM2 macrophages and fibrotic progression in SSc-ILD. This schematic illustrates the proposed mechanism by which GM-CSF–induced monocyte-derived macrophages differentiate and promote lung fibrosis in patients with SSc-ILD. In SSc-ILD, recruited monocytes stimulated by GM-CSF upregulate TREM2 and GPNMB , leading to increased secretion of cytokines such as CCL2 and TGF-β1. CCL2 promotes additional recruitment of monocytes via the CCL2-CCR2 axis. These TREM2 + macrophages enhance fibroblast activation through TGF-β1 production, driving fibroblast to myofibroblast differentiation and contributing to fibrotic remodeling in the lung.

    Article Snippet: Macrophages differentiated from monocyte subsets by GM-CSF from SSc-ILD patients were cultured for 7 days and subsequently co-cultured with commercially sourced human lung fibroblasts (ACBR 469, Cell Systems, Kirkland, WA, USA) for 5 days, with or without treatment with a TREM2 inhibitor (BLP-NR018, Alomone Labs, Jerusalem, Israel).

    Techniques: Derivative Assay, Activation Assay

    A) Hydrogels were composed of either 0% or 50% mixture of tyramine-modified silk and were exposed to media without or with 5 ng/mL TGFβ. After hydrogels were cast, 25,000 NHLF cells were seeded on the surface. B) SEM imaging of the surface of the silk hydrogels incubated without cells for Day 0 and Day 14. C) Live/Dead imaging of Calcein AM for live cells (green) and Ethidium Homodimer-1 for dead cells (red) indicated cytocompatibility. D) Alamar Blue Assay for metabolic activity indicated that 0% gels showed an increase in activity over 14 days, while 50% gels plateaued from day 7 to 14. E) Mammalian β-Galactosidase Assay for senescence revealed no change for any timepoints tested over 14 days. N=3-4, Error bars = SEM.TCP = Tissue Culture Plate, T-= without TGFβ, T+ = 5 ng/mL of TGFβ. Two-way ANOVA, Tukey’s: ns = not significant p > 0.05, * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001.

    Journal: bioRxiv

    Article Title: Progressive matrix stiffening of tyramine-modified silk fibroin hydrogels governs stage-specific pulmonary fibroblast activation

    doi: 10.64898/2026.06.01.729382

    Figure Lengend Snippet: A) Hydrogels were composed of either 0% or 50% mixture of tyramine-modified silk and were exposed to media without or with 5 ng/mL TGFβ. After hydrogels were cast, 25,000 NHLF cells were seeded on the surface. B) SEM imaging of the surface of the silk hydrogels incubated without cells for Day 0 and Day 14. C) Live/Dead imaging of Calcein AM for live cells (green) and Ethidium Homodimer-1 for dead cells (red) indicated cytocompatibility. D) Alamar Blue Assay for metabolic activity indicated that 0% gels showed an increase in activity over 14 days, while 50% gels plateaued from day 7 to 14. E) Mammalian β-Galactosidase Assay for senescence revealed no change for any timepoints tested over 14 days. N=3-4, Error bars = SEM.TCP = Tissue Culture Plate, T-= without TGFβ, T+ = 5 ng/mL of TGFβ. Two-way ANOVA, Tukey’s: ns = not significant p > 0.05, * = p < 0.05, ** = p < 0.01, *** = p < 0.001, **** = p < 0.0001.

    Article Snippet: Normal human lung fibroblasts (NHLFs, PCS-201-013, ATCC, Manassas, VA, USA) were cultured in Dulbecco’s Modified Eagle Medium, high glucose (DMEM, ThermoFisher) supplemented with 10% Gibco Fetal Bovine Serum, Premium (FBS, ThermoFisher), 1% Gibco non-essential amino acids (ThermoFisher), and 1% Gibco antibiotic–antimycotic (ThermoFisher).

    Techniques: Modification, Imaging, Incubation, Alamar Blue Assay, Activity Assay

    Top row: NHLFs on 0% SF-TA hydrogels at Day 2, Day 7, and Day 14, exhibiting a proliferative, inflammatory phenotype consistent with early fibroblast activation, characterized by secretion of IL-6, IL-8, and MCP-1 (dots) and progressive collagen deposition (fibers). Bottom row: NHLFs on 50% SF-TA hydrogels at Day 2, Day 7, and Day 14, exhibiting metabolic plateau and lower inflammatory cytokine secretion, gradual collagen secretion, with TGFβ-dependent myofibroblast activation. Together, these two substrate conditions recapitulate distinct stages of the fibrotic disease continuum.

    Journal: bioRxiv

    Article Title: Progressive matrix stiffening of tyramine-modified silk fibroin hydrogels governs stage-specific pulmonary fibroblast activation

    doi: 10.64898/2026.06.01.729382

    Figure Lengend Snippet: Top row: NHLFs on 0% SF-TA hydrogels at Day 2, Day 7, and Day 14, exhibiting a proliferative, inflammatory phenotype consistent with early fibroblast activation, characterized by secretion of IL-6, IL-8, and MCP-1 (dots) and progressive collagen deposition (fibers). Bottom row: NHLFs on 50% SF-TA hydrogels at Day 2, Day 7, and Day 14, exhibiting metabolic plateau and lower inflammatory cytokine secretion, gradual collagen secretion, with TGFβ-dependent myofibroblast activation. Together, these two substrate conditions recapitulate distinct stages of the fibrotic disease continuum.

    Article Snippet: Normal human lung fibroblasts (NHLFs, PCS-201-013, ATCC, Manassas, VA, USA) were cultured in Dulbecco’s Modified Eagle Medium, high glucose (DMEM, ThermoFisher) supplemented with 10% Gibco Fetal Bovine Serum, Premium (FBS, ThermoFisher), 1% Gibco non-essential amino acids (ThermoFisher), and 1% Gibco antibiotic–antimycotic (ThermoFisher).

    Techniques: Activation Assay