Review

tlr5 antibodies (Cell Signaling Technology Inc)

Cell Signaling Technology Inc is a verified supplier

Cell Signaling Technology Inc manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cell Signaling Technology Inc tlr5 antibodies
Tlr5 Antibodies, supplied by Cell Signaling Technology Inc, 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/product/tlr5+antibodies/pm41904635-83-7-9
Average 86 stars, based on 1 article reviews

tlr5 antibodies - by Bioz Stars, 2026-09

86/100 stars

Images

Western Blot:

Article Title: Clostridioides difficile-Derived Extracellular Vesicles Induce Proinflammatory Responses in Macrophages.
Article Snippet: .. For Western blot analysis, two distinct anti ‐TLR5 antibodies (CST, USA and Epizyme, China) were used to confirm protein loss (Figure S1 ). ..

Image Search Results

a , Quantitative PCR of TLR5 from whole liver biopsy tissue, grouped by histological stage (ctrl n=5, steatosis n=9, MASH F1-2 n=5, MASH F3-4 n=5). b , Representative images of immunofluorescence of human liver biopsy tissue (n=12) showing TLR5 (green), albumin (grey), α-SMA (red), Hoescht (blue) in control (top row) and MASH with F3 fibrosis (bottom row) (Scale bar 200µm). c , NanoString CosMX analysis of explant liver tissue from MASH advanced fibrosis. Red dots represent TLR5 expressing cells. d , Zoomed representative images of immunofluorescence staining of human liver biopsy tissue showing TLR5 (green) and α-SMA (red) in MASH F3 (n=12,scale bar 100µm). e , f , Kaplan–Meier curves for liver-related events and all-cause mortality stratified by hepatic TLR5 expression in the SteatoSITE cohort. Error bars represent mean±standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: a , Quantitative PCR of TLR5 from whole liver biopsy tissue, grouped by histological stage (ctrl n=5, steatosis n=9, MASH F1-2 n=5, MASH F3-4 n=5). b , Representative images of immunofluorescence of human liver biopsy tissue (n=12) showing TLR5 (green), albumin (grey), α-SMA (red), Hoescht (blue) in control (top row) and MASH with F3 fibrosis (bottom row) (Scale bar 200µm). c , NanoString CosMX analysis of explant liver tissue from MASH advanced fibrosis. Red dots represent TLR5 expressing cells. d , Zoomed representative images of immunofluorescence staining of human liver biopsy tissue showing TLR5 (green) and α-SMA (red) in MASH F3 (n=12,scale bar 100µm). e , f , Kaplan–Meier curves for liver-related events and all-cause mortality stratified by hepatic TLR5 expression in the SteatoSITE cohort. Error bars represent mean±standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Real-time Polymerase Chain Reaction, Immunofluorescence, Control, Expressing, Staining, Standard Deviation

a , Publicly-available single nucleus RNA sequencing data from 47 liver biopsies from individuals with different stages of MASLD (Gribben et al. Nature 2024, PMID 38778114 ) were analysed. Pie chart demonstrates proportion of TLR5 expressing single cells (n=1609) that co-expressed albumin (ALB, n=1495), equating to 92.9% derived from albumin-expressing hepatocytes. b , Liver TLR5 mRNA expression in SteatoSITE cohort divided according to histological MASLD disease severity. c , Liver TLR4 mRNA expression in SteatoSITE cohort divided according to histological MASLD disease severity. d, Liver TLR2 mRNA expression in SteatoSITE cohort divided according to histological MASLD disease severity. e , All-cause mortality by TLR5 expression in SteatoSITE cohort with MASH fibrosis stage 0 – 2. f , All-cause mortality by TLR5 expression in SteatoSITE cohort with MASH fibrosis stage 3 – 4. Kaplan–Meier curves for all-cause mortality stratified by hepatic TLR5 expression. P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: a , Publicly-available single nucleus RNA sequencing data from 47 liver biopsies from individuals with different stages of MASLD (Gribben et al. Nature 2024, PMID 38778114 ) were analysed. Pie chart demonstrates proportion of TLR5 expressing single cells (n=1609) that co-expressed albumin (ALB, n=1495), equating to 92.9% derived from albumin-expressing hepatocytes. b , Liver TLR5 mRNA expression in SteatoSITE cohort divided according to histological MASLD disease severity. c , Liver TLR4 mRNA expression in SteatoSITE cohort divided according to histological MASLD disease severity. d, Liver TLR2 mRNA expression in SteatoSITE cohort divided according to histological MASLD disease severity. e , All-cause mortality by TLR5 expression in SteatoSITE cohort with MASH fibrosis stage 0 – 2. f , All-cause mortality by TLR5 expression in SteatoSITE cohort with MASH fibrosis stage 3 – 4. Kaplan–Meier curves for all-cause mortality stratified by hepatic TLR5 expression. P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: RNA Sequencing, Expressing, Derivative Assay

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet:

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Expressing

Primary hepatocytes treated with oleic acid and palmitic acid (OA PA), flagellin or combination (OA PA + flagellin) for 24 hours a, in the presence or absence of 1µM TH1020 (TLR5 inhibitor) , 5µg/mL Pab hTLR4 (TLR4 inhibitor), 5µg/mL Pab hTLR2 (TLR2 inhibitor), b - f in the presence or absence of 1µM TH1020. a , IL-8 concentration (n=3–4 replicates per condition). b , Representative images of lipid deposition quantified using BODIPY 493/503 staining (green), nuclei stained with DAPI (blue) via confocal microscopy (Scale bars 50μm) and BODIPY quantified according to relative intensity/DAPI. Experiments performed in triplicates for each condition. c - e Expression of fatty acid oxidation enzymes: c, very long chain specific acyl-CoA dehydrogenase – ACADVL, d, medium-chain specific acyl-CoA dehydrogenase - ACADM and e, long-chain 3-hydroxyl-CoA dehydrogenase – HADHA. f , DNA damage-inducible transcript 3 (DDIT3) concentration (n=2 independent experiments). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple. ANOVA, analysis of variance; Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: Primary hepatocytes treated with oleic acid and palmitic acid (OA PA), flagellin or combination (OA PA + flagellin) for 24 hours a, in the presence or absence of 1µM TH1020 (TLR5 inhibitor) , 5µg/mL Pab hTLR4 (TLR4 inhibitor), 5µg/mL Pab hTLR2 (TLR2 inhibitor), b - f in the presence or absence of 1µM TH1020. a , IL-8 concentration (n=3–4 replicates per condition). b , Representative images of lipid deposition quantified using BODIPY 493/503 staining (green), nuclei stained with DAPI (blue) via confocal microscopy (Scale bars 50μm) and BODIPY quantified according to relative intensity/DAPI. Experiments performed in triplicates for each condition. c - e Expression of fatty acid oxidation enzymes: c, very long chain specific acyl-CoA dehydrogenase – ACADVL, d, medium-chain specific acyl-CoA dehydrogenase - ACADM and e, long-chain 3-hydroxyl-CoA dehydrogenase – HADHA. f , DNA damage-inducible transcript 3 (DDIT3) concentration (n=2 independent experiments). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple. ANOVA, analysis of variance; Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Concentration Assay, Staining, Confocal Microscopy, Expressing, Standard Deviation

a , HepG2 cells, b , Huh7 cells, treated with oleic acid and palmitic acid (OA PA), flagellin or combination (OA PA + flagellin) for 24 hours in the presence or absence of 1µM TH1020 (TLR5 inhibitor). Representative images of lipid deposition quantified using BODIPY 493/503 staining (green), nuclei stained with DAPI (blue) via confocal microscopy (Scale bars 50µm). Experiments performed in triplicates for each condition. c – h, Expression of fatty acid oxidation enzymes ( c – e in HepG2 cells, f – h in Huh7 cells) of very long chain specific acyl-CoA dehydrogenase – ACADVL, medium-chain specific acyl-CoA dehydrogenase - ACADM and long-chain 3-hydroxyl-CoA dehydrogenase – HADHA following treatment with OA PA, flagellin or combination (OA PA flagellin) for 24 hours in the presence or absence of 1µM TH1020 (n=2 independent experiments). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: a , HepG2 cells, b , Huh7 cells, treated with oleic acid and palmitic acid (OA PA), flagellin or combination (OA PA + flagellin) for 24 hours in the presence or absence of 1µM TH1020 (TLR5 inhibitor). Representative images of lipid deposition quantified using BODIPY 493/503 staining (green), nuclei stained with DAPI (blue) via confocal microscopy (Scale bars 50µm). Experiments performed in triplicates for each condition. c – h, Expression of fatty acid oxidation enzymes ( c – e in HepG2 cells, f – h in Huh7 cells) of very long chain specific acyl-CoA dehydrogenase – ACADVL, medium-chain specific acyl-CoA dehydrogenase - ACADM and long-chain 3-hydroxyl-CoA dehydrogenase – HADHA following treatment with OA PA, flagellin or combination (OA PA flagellin) for 24 hours in the presence or absence of 1µM TH1020 (n=2 independent experiments). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Staining, Confocal Microscopy, Expressing, Standard Deviation

DNA damage-inducible transcript 3 (DDIT3) concentration in a , HepG2 cells; b , Huh7 cells, treated with oleic acid and palmitic acid (OA PA), flagellin or combination (OA PA + flagellin) for 24 hours in the presence or absence of 1µM TH1020 (TLR5 inhibitor) (n=2 independent experiments). c , d , IL-8 concentration in c , HepG2 cells, d , Huh7 cells, treated with OA PA for 24 hours in the presence or absence of 27µM CU-CPT4a (TLR3 inhibitor), 5µg/mL PAb hTLR4 (TLR5 inhibitor), 1µM TH1020 (n=3 independent experiments). e , Flagellin concentration conditioned media from primary hepatocytes treated for 24 hours treatment with OA PA compared to control (n=3 independent experiments). f , IL-8 concentration in primary hepatocytes treated with 250µM oleic acid 125µM palmitic acid (OA PA), 25ng/mL flagellin or combination (OA PA + flagellin) for 24 hours (n=2 independent experiments). g , IL-8 concentration in HEK cells treated with OA PA, flagellin, and combination (OA PA + flagellin) for 24 hours (n=3 independent experiments). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: DNA damage-inducible transcript 3 (DDIT3) concentration in a , HepG2 cells; b , Huh7 cells, treated with oleic acid and palmitic acid (OA PA), flagellin or combination (OA PA + flagellin) for 24 hours in the presence or absence of 1µM TH1020 (TLR5 inhibitor) (n=2 independent experiments). c , d , IL-8 concentration in c , HepG2 cells, d , Huh7 cells, treated with OA PA for 24 hours in the presence or absence of 27µM CU-CPT4a (TLR3 inhibitor), 5µg/mL PAb hTLR4 (TLR5 inhibitor), 1µM TH1020 (n=3 independent experiments). e , Flagellin concentration conditioned media from primary hepatocytes treated for 24 hours treatment with OA PA compared to control (n=3 independent experiments). f , IL-8 concentration in primary hepatocytes treated with 250µM oleic acid 125µM palmitic acid (OA PA), 25ng/mL flagellin or combination (OA PA + flagellin) for 24 hours (n=2 independent experiments). g , IL-8 concentration in HEK cells treated with OA PA, flagellin, and combination (OA PA + flagellin) for 24 hours (n=3 independent experiments). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Concentration Assay, Control, Standard Deviation

a , HEK-Blue™ hTLR5 cells treated with oleic acid and palmitic acid (OA PA), flagellin for 24 hours. TLR5 ligand activity assessed by optical density measurements of SEAP production. n=3 independent experiments. b , Primary hepatocytes treated with OA PA for 24 hours in the presence or absence of fatty acid transporter protein inhibitor cocktail (10µM obeticholic acid (FATP5 inhibitor), 80µM SML2148 (CD36 inhibitor), 50µM Lipofermata (FATP2 inhibitor)). Representative images of lipid deposition quantified using BODIPY 493/503 staining (green), nuclei stained with DAPI (blue) via confocal microscopy (Scale bars 50µm). Experiments performed in triplicate for each condition. c – e , IL-8 concentrations in c, Huh7 cells treated with OA PA for 24 hours in the presence or absence of 16µM SML2148, 10µM Lipofermata, 2µM obeticholic acid, combination of 16µM SML2148, 10µM Lipofermata and 2µM obeticholic acid in a cocktail, 1µM TH1020 (TLR5 inhibitor) with 10µM Lipofermata (n=3 independent experiments). d , Primary hepatocytes treated with OA PA for 24 hours in the presence or absence of 40µM Pepinh-TRIF (TRIF inhibitor), 40µM TJ-M2010-5 (MyD88 inhibitor) (n=2 independent experiments) and e , HepG2 cells treated with OA PA for 24 hours in the presence or absence of 5µM (5Z)-7-Oxozeaenol (TAK1 inhibitor) (n=3 independent experiments). f, Schematic diagram depicting TLR5 signalling in hepatocytes (created using Biorender). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: a , HEK-Blue™ hTLR5 cells treated with oleic acid and palmitic acid (OA PA), flagellin for 24 hours. TLR5 ligand activity assessed by optical density measurements of SEAP production. n=3 independent experiments. b , Primary hepatocytes treated with OA PA for 24 hours in the presence or absence of fatty acid transporter protein inhibitor cocktail (10µM obeticholic acid (FATP5 inhibitor), 80µM SML2148 (CD36 inhibitor), 50µM Lipofermata (FATP2 inhibitor)). Representative images of lipid deposition quantified using BODIPY 493/503 staining (green), nuclei stained with DAPI (blue) via confocal microscopy (Scale bars 50µm). Experiments performed in triplicate for each condition. c – e , IL-8 concentrations in c, Huh7 cells treated with OA PA for 24 hours in the presence or absence of 16µM SML2148, 10µM Lipofermata, 2µM obeticholic acid, combination of 16µM SML2148, 10µM Lipofermata and 2µM obeticholic acid in a cocktail, 1µM TH1020 (TLR5 inhibitor) with 10µM Lipofermata (n=3 independent experiments). d , Primary hepatocytes treated with OA PA for 24 hours in the presence or absence of 40µM Pepinh-TRIF (TRIF inhibitor), 40µM TJ-M2010-5 (MyD88 inhibitor) (n=2 independent experiments) and e , HepG2 cells treated with OA PA for 24 hours in the presence or absence of 5µM (5Z)-7-Oxozeaenol (TAK1 inhibitor) (n=3 independent experiments). f, Schematic diagram depicting TLR5 signalling in hepatocytes (created using Biorender). Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Activity Assay, Staining, Confocal Microscopy, Standard Deviation

a , b , IL-8 concentration in a , HepG2 cells; b , Huh7 cells, treated with oleic acid and palmitic acid (OA PA) for 24 hours in the presence or absence of 40µM Pepinh-TRIF (TRIF inhibitor) (n=3 independent experiments). c , IL-8 concentration in HepG2 cells treated with OA PA for 24 hours in the presence or absence of 40µM TJ-M2010-5 (MyD88 inhibitor) (n=3 independent experiments). IL-8 concentration in Huh7 cells treated with OA PA for 24 hours in the presence or absence of 5µM (5Z)-7-Oxozeaenol (TAK1 inhibitor) (n=3 independent experiments). e , TGFβ1 concentration in LX2 cells following 24 hours treatment with conditioned media from primary hepatocytes treated with OA PA, flagellin in the presence or absence of 1µM TH1020 (TLR5 inhibitor) (n=3 replicates per condition). P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: a , b , IL-8 concentration in a , HepG2 cells; b , Huh7 cells, treated with oleic acid and palmitic acid (OA PA) for 24 hours in the presence or absence of 40µM Pepinh-TRIF (TRIF inhibitor) (n=3 independent experiments). c , IL-8 concentration in HepG2 cells treated with OA PA for 24 hours in the presence or absence of 40µM TJ-M2010-5 (MyD88 inhibitor) (n=3 independent experiments). IL-8 concentration in Huh7 cells treated with OA PA for 24 hours in the presence or absence of 5µM (5Z)-7-Oxozeaenol (TAK1 inhibitor) (n=3 independent experiments). e , TGFβ1 concentration in LX2 cells following 24 hours treatment with conditioned media from primary hepatocytes treated with OA PA, flagellin in the presence or absence of 1µM TH1020 (TLR5 inhibitor) (n=3 replicates per condition). P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Concentration Assay

Normalised RNA counts for TLR5 and TLR4 extracted from primary human hepatic stellate cells isolated from non-fibrotic, non-steatotic human livers (n=19). b , TGFβ1 concentration c , Pro-collagen 1⍺1 concentration, in LX2 cells treated with oleic acid and palmitic acid (OA PA), flagellin for 24 hours (n=3 independent experiments). d , TGFβ1 concentration, e , Pro-collagen 1⍺1 concentration, in LX2 cells treated with conditioned media from HepG2 cells treated with OA PA, flagellin in the presence or absence of 1µM TH1020 (TLR5 inhibitor) (n=3 independent experiments). Schematic diagram created using Biorender. Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: Normalised RNA counts for TLR5 and TLR4 extracted from primary human hepatic stellate cells isolated from non-fibrotic, non-steatotic human livers (n=19). b , TGFβ1 concentration c , Pro-collagen 1⍺1 concentration, in LX2 cells treated with oleic acid and palmitic acid (OA PA), flagellin for 24 hours (n=3 independent experiments). d , TGFβ1 concentration, e , Pro-collagen 1⍺1 concentration, in LX2 cells treated with conditioned media from HepG2 cells treated with OA PA, flagellin in the presence or absence of 1µM TH1020 (TLR5 inhibitor) (n=3 independent experiments). Schematic diagram created using Biorender. Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Isolation, Concentration Assay, Standard Deviation

Schematic representation of precision-cut liver slices (PCLS) setup, created in Biorender. PCLS were cultured for 16 hours in the presence or absence of 1µM TH1020 (TLR5 inhibitor) and treated with bovine serum albumin (BSA) or oleic acid and palmitic acid (OA PA) for 24 hours (n=3). Representative immunohistochemistry images H&E and Collagen III quantification (% area) of PCLS shown. Scale bar 100µM and 50µM. Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Journal: bioRxiv

Article Title: TLR5 drives metabolic dysfunction-associated steatohepatitis through lipid- and flagellin-induced hepatocyte injury signalling

doi: 10.64898/2026.02.05.703969

Figure Lengend Snippet: Schematic representation of precision-cut liver slices (PCLS) setup, created in Biorender. PCLS were cultured for 16 hours in the presence or absence of 1µM TH1020 (TLR5 inhibitor) and treated with bovine serum albumin (BSA) or oleic acid and palmitic acid (OA PA) for 24 hours (n=3). Representative immunohistochemistry images H&E and Collagen III quantification (% area) of PCLS shown. Scale bar 100µM and 50µM. Error bars represent mean ± standard deviation; P values determined by t test or ANOVA with post-test multiple comparisons. ANOVA, analysis of variance. Only statistically significant comparisons (p<0.05) are highlighted.

Article Snippet: For TLR5 inhibition, liver slices were incubated with 1 μM TLR5 antagonist, TH1020, (HY-116961-5, MedChemexpress) for 16 hours.

Techniques: Cell Culture, Immunohistochemistry, Standard Deviation

LPS and flagellin induce DNA double-strand breaks in breast acini in a TLR-dependent manner. A. Representative comet images from neutral comet assays performed on 3D cultures of breast acini treated with vehicle (control), 1 μg/ml LPS, 1 μg/ml LTA, and 10 ng/ml flagellin for 72 h. Bleomycin (BLM; 20 mU/ml; 2h) was used as positive control. B. Comet assay quantification. n=300 acini from 3 biological replicates. C. Representative images for immunofluorescence staining of 53BP1 (red) in acini treated with MAMPs ± TLR inhibitors. Nuclei are counterstained with DAPI (blue). D-F. Quantification of 53BP1 foci numbers in acini treated with LPS ± TLR4 inhibitor (D), with LTA ± TLR2 inhibitor (E) or with flagellin ± TLR5 inhibitor (F). ns is not significant. *P<0.05, **P<0.01, ***P<0.001.

Journal: Neoplasia (New York, N.Y.)

Article Title: Microbe-associated molecular patterns differentially mediate carcinogenic alterations of the breast tissue in the context of obesity

doi: 10.1016/j.neo.2026.101284

Figure Lengend Snippet: LPS and flagellin induce DNA double-strand breaks in breast acini in a TLR-dependent manner. A. Representative comet images from neutral comet assays performed on 3D cultures of breast acini treated with vehicle (control), 1 μg/ml LPS, 1 μg/ml LTA, and 10 ng/ml flagellin for 72 h. Bleomycin (BLM; 20 mU/ml; 2h) was used as positive control. B. Comet assay quantification. n=300 acini from 3 biological replicates. C. Representative images for immunofluorescence staining of 53BP1 (red) in acini treated with MAMPs ± TLR inhibitors. Nuclei are counterstained with DAPI (blue). D-F. Quantification of 53BP1 foci numbers in acini treated with LPS ± TLR4 inhibitor (D), with LTA ± TLR2 inhibitor (E) or with flagellin ± TLR5 inhibitor (F). ns is not significant. *P<0.05, **P<0.01, ***P<0.001.

Article Snippet: Antibodies against TLR4 (Santa Cruz; sc-293072), TLR5 (Santa Cruz; sc-518106), TLR2 (Santa Cruz; sc-21795), NF-κB p65 (Cell Signaling Technology; 8242), LEDGF (Cell Signaling Technology; 2088), Lamin B (Abcam; Ab16048), and α-tubulin (Cell Signaling Technology; 2144) were used.

Techniques: Control, Positive Control, Single Cell Gel Electrophoresis, Immunofluorescence, Staining

Blockade of TLR4 and TLR5 mitigates DNA damage in the mammary glands. A. Schematic of the experiment. B-D-F. Representative images for TLR2 (B), TLR4 (D), and TLR5 (F) IHC signals in mammary glands of mice treated with saline, mismatch morpholino (MM) and the corresponding TLR morpholino (TLR M). Hematoxylin was used as a counterstain. Image analysis and quantification of TLR2/4/5-DAB positive areas is shown in the graphs (C,E,G). H. Representative comet images of the neutral comet assay performed on mammary cells treated with vehicle, MM, and TLR morpholinos. I. Quantification of comet assay results for the aforementioned mice groups. ns is not significant. *P<0.05, **P<0.01.

Journal: Neoplasia (New York, N.Y.)

Article Title: Microbe-associated molecular patterns differentially mediate carcinogenic alterations of the breast tissue in the context of obesity

doi: 10.1016/j.neo.2026.101284

Figure Lengend Snippet: Blockade of TLR4 and TLR5 mitigates DNA damage in the mammary glands. A. Schematic of the experiment. B-D-F. Representative images for TLR2 (B), TLR4 (D), and TLR5 (F) IHC signals in mammary glands of mice treated with saline, mismatch morpholino (MM) and the corresponding TLR morpholino (TLR M). Hematoxylin was used as a counterstain. Image analysis and quantification of TLR2/4/5-DAB positive areas is shown in the graphs (C,E,G). H. Representative comet images of the neutral comet assay performed on mammary cells treated with vehicle, MM, and TLR morpholinos. I. Quantification of comet assay results for the aforementioned mice groups. ns is not significant. *P<0.05, **P<0.01.

Techniques: Saline, Neutral Comet Assay, Single Cell Gel Electrophoresis

Intestinal permeability and expression of flagellin and TLR5 protein in the lamina propria of the mucosa of rats in various groups. FITC-Dextran was used to detect the intestinal permeability of rats and laser confocal microscopy was employed to observe the localization of flagellin and TLR5 proteins of colon three repeated tests. (Adopt Tukey statistical method. Refer to the annotations in the reference image for grouping identification.)

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: The effect of Massa Medicata Fermentata on the cytokine secretion of colonic mucosa and visceral sensitivity in rats with IBS-D

doi: 10.3389/fcimb.2025.1616796

Figure Lengend Snippet: Intestinal permeability and expression of flagellin and TLR5 protein in the lamina propria of the mucosa of rats in various groups. FITC-Dextran was used to detect the intestinal permeability of rats and laser confocal microscopy was employed to observe the localization of flagellin and TLR5 proteins of colon three repeated tests. (Adopt Tukey statistical method. Refer to the annotations in the reference image for grouping identification.)

Article Snippet: MMF (China Resources Sanjiu Co., Ltd); glacial acetic acid (10000208 Sinopharm, Inc.); FITC-Dextran (Sigma, Inc.); WB Antibodies: TLR5 Antibody (rabbit source, Proteintech, Inc.), TRIF Antibody (rabbit source, Affinity, Inc.); P-ERK1/2 Antibody (rabbit source, abcam, Inc.); immunofluorescent antibodies: immunofluorescent primary antibody: TLR5 (rabbit source, Three Eagles, Inc.), immunofluorescent primary antibody: Flic (mouse source, Yiqiao, Inc.), and Immunofluorescence secondary antibody: goat anti-rabbit IgGH&L (Cy3) (abcam, Inc.), immunofluorescence secondary antibody: goat anti-mouse IgGH&L (FITC) (abcam, Inc.); Immunohistochemistry antibody: immunohistochemistry primary antibody: TLR5 (rabbit source, proteintech, Inc.), immunohistochemistry primary antibody: TRIF (rabbit source, Affinity, Inc.), the Immunohistochemical primary antibody: p-ERK1/2 (rabbit source abcam), immunohistochemical secondary antibody: HRP-labeled goat anti-rabbit IgG (Biyun Tian, Inc.); Percoll lymphocyte isolate P8370 (Solarbio, Inc.); LPDCs magnetic bead sorting kit (OX62) (MiltenyiBiotec, Inc.) Anti-RatCD103, PE (Bioscience, Inc.); Rat spleen lymphocyte isolate LTS1083PK-200 (TBD, Inc.); CD4 Magnetic Bead Sorting Kit (MiltenyiBiotec, Inc.); CD4MonoclonalAntibody;CCK-8 Kit C0039 (Biotronix, Inc.); Rat Interleukin 12 (IL-12) ELISA Kit, Rat Interferon Gamma (IFN-γ) ELISA Kit, Rat Interleukin 4 (IL-4) ELISA Kit, Rat Interleukin 9 (IL-9) kit, Rat Interleukin 6 (IL-6) ELISA kit, Rat Interleukin 17A (IL-17A) ELISA kit, Rat Transforming Growth Factor β (TGF-β) ELISA kit (Jiangsu Jingmei, Inc.).

Techniques: Permeability, Expressing, Confocal Microscopy

Expression of TLR5, TRIF and p-EPK1/2 in LPDCs of rats in each group. The mRNA expression of TLR5, TRIF, and p-EPK1/2 in LPDCs was detected by qPCR. The expression of TLR5, TRIF, and p-EPK1/2 proteins in LPDCs of rats in each group was detected by WB three repeated tests. (Adopt Tukey statistical method. Refer to the annotations in the reference image for grouping identification.)

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: The effect of Massa Medicata Fermentata on the cytokine secretion of colonic mucosa and visceral sensitivity in rats with IBS-D

doi: 10.3389/fcimb.2025.1616796

Figure Lengend Snippet: Expression of TLR5, TRIF and p-EPK1/2 in LPDCs of rats in each group. The mRNA expression of TLR5, TRIF, and p-EPK1/2 in LPDCs was detected by qPCR. The expression of TLR5, TRIF, and p-EPK1/2 proteins in LPDCs of rats in each group was detected by WB three repeated tests. (Adopt Tukey statistical method. Refer to the annotations in the reference image for grouping identification.)

Techniques: Expressing

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: The effect of Massa Medicata Fermentata on the cytokine secretion of colonic mucosa and visceral sensitivity in rats with IBS-D

doi: 10.3389/fcimb.2025.1616796

Techniques: Permeability, Expressing, Confocal Microscopy

Journal: Frontiers in Cellular and Infection Microbiology

Article Title: The effect of Massa Medicata Fermentata on the cytokine secretion of colonic mucosa and visceral sensitivity in rats with IBS-D

doi: 10.3389/fcimb.2025.1616796

Techniques: Expressing

Review

tlr5 antibodies (Cell Signaling Technology Inc)

Structured Review

Images

Related Articles

Western Blot:

Similar Products

Image Search Results