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human il 17a  (R&D Systems)


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    Structured Review

    R&D Systems human il 17a
    Human Il 17a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 112 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human il 17a/product/R&D Systems
    Average 95 stars, based on 112 article reviews
    human il 17a - by Bioz Stars, 2026-06
    95/100 stars

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    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
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    TargetMol recombinant mouse il 17a protein
    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
    Recombinant Mouse Il 17a Protein, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TargetMol recombinant human il 17a protein
    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
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    Average 94 stars, based on 1 article reviews
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    MedChemExpress recombinant mouse il 17a
    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
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    Average 93 stars, based on 1 article reviews
    recombinant mouse il 17a - by Bioz Stars, 2026-06
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    R&D Systems human il 17a
    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
    Human Il 17a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Novoprotein recombinant human il 17a
    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
    Recombinant Human Il 17a, supplied by Novoprotein, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    95
    R&D Systems il17a
    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection <t>increases</t> <t>IL-17A</t> content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway
    Il17a, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/il17a/product/R&D Systems
    Average 95 stars, based on 1 article reviews
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    MedChemExpress recombinant il 17a
    Gut microbiota drive neutrophil recruitment via <t>a</t> <t>IL-17A</t> dependent pathway. The experimental aimed to explore the role of IL-17A in the gut microbiota-mediated enhancement of host resistance against systemic S. aureus infection. The experimental utilized WT mice assigned to No ABX, ABX, and FMT groups, as well as Il17a −/− mice assigned to No ABX and ABX groups. (A) WT mice were i.v . injected with S. aureus USA300, the level of IL-17A was determined in liver tissues by ELISA at 0, 6, 12, and 24 hours post-infection ( n = 5). (B-E) Hepatic IL-17A, KC, MIP-2, and MPO levels in No ABX, ABX, and FMT mice were measured by ELISA at 12 hours post-infection ( n = 5). (F) Schematic shows that Il17a −/− mice were pretreated with either No ABX or ABX containing water. Subsequently, along with the WT-No ABX group, all mice were challenged i.v . with S. aureus USA300. (G) Survival curves of WT-No ABX, Il17a −/− -No ABX, and Il17a −/− - ABX mice after i.v . challenged with S. aureus ( n = 10). (H) Bacterial burden in livers of WT-No ABX, Il17a −/− -No ABX, and Il17a −/− - ABX mice at 12 hours post-infection ( n = 7). (I) Representative contour plots of neutrophils (CD3 − CD11b + Ly6G + ) in liver at 12 hours post-infection. (J) Scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection. ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.
    Recombinant Il 17a, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/recombinant il 17a/product/MedChemExpress
    Average 97 stars, based on 1 article reviews
    recombinant il 17a - by Bioz Stars, 2026-06
    97/100 stars
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    Image Search Results


    Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection increases IL-17A content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway

    Journal: Journal of Animal Science and Biotechnology

    Article Title: Baicalin alleviates mastitis in dairy cows by targeting IL-17RA to inhibit IL-17 signaling pathway activation

    doi: 10.1186/s40104-026-01401-2

    Figure Lengend Snippet: Schematic overview of baicalin's mechanism in alleviating mastitis by regulating the IL-17RA-mediated IL-17 signaling pathway. A Oral administration of baicalin to mice and dairy cows. B In vivo release of LPS by E. coli . C LPS activated the TLR4/MyD88/NF-κB pathway in epithelial cells. D NF-κB was activated within the cell nucleus. E E. coli infection increases IL-17A content in mammary glands. F IL-17A binds to IL-17RA on the cell membrane surface, thereby activating the IL-17 signaling pathway. G Activation of the MAPK signaling pathway and ERK signaling pathway. H Production of IL-6, TNFα and IL-1β. I TNFα activated TNF signaling pathway. J TJ structure damage. K Baicalin inhibits IL-17RA signal transduction, thereby preventing activation of the IL-17 signaling pathway

    Article Snippet: An in vitro mastitis model was established by treating cells with 5 μg/mL LPS (Sigma, USA) for 12 h. Baicalin (purity ≥ 95%) was purchased from Macklin (Shanghai, China), with a concentration of 20 μmol/L for 24 h. Furthermore, the TNFα inhibitor SPD304 and recombinant IL-17A (rIL-17A) were purchased from MedChemExpress (MCE, USA) and were used at concentrations of 5 μmol/L (for 2 h) and 100 ng/mL (for 12 h), respectively.

    Techniques: In Vivo, Infection, Membrane, Activation Assay, Transduction

    Gut microbiota drive neutrophil recruitment via a IL-17A dependent pathway. The experimental aimed to explore the role of IL-17A in the gut microbiota-mediated enhancement of host resistance against systemic S. aureus infection. The experimental utilized WT mice assigned to No ABX, ABX, and FMT groups, as well as Il17a −/− mice assigned to No ABX and ABX groups. (A) WT mice were i.v . injected with S. aureus USA300, the level of IL-17A was determined in liver tissues by ELISA at 0, 6, 12, and 24 hours post-infection ( n = 5). (B-E) Hepatic IL-17A, KC, MIP-2, and MPO levels in No ABX, ABX, and FMT mice were measured by ELISA at 12 hours post-infection ( n = 5). (F) Schematic shows that Il17a −/− mice were pretreated with either No ABX or ABX containing water. Subsequently, along with the WT-No ABX group, all mice were challenged i.v . with S. aureus USA300. (G) Survival curves of WT-No ABX, Il17a −/− -No ABX, and Il17a −/− - ABX mice after i.v . challenged with S. aureus ( n = 10). (H) Bacterial burden in livers of WT-No ABX, Il17a −/− -No ABX, and Il17a −/− - ABX mice at 12 hours post-infection ( n = 7). (I) Representative contour plots of neutrophils (CD3 − CD11b + Ly6G + ) in liver at 12 hours post-infection. (J) Scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection. ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Journal: Virulence

    Article Title: Gut microbiota-driven IL-17A production by hepatic γδ T cells enhances neutrophil defense against systemic Staphylococcus aureus infection

    doi: 10.1080/21505594.2026.2629132

    Figure Lengend Snippet: Gut microbiota drive neutrophil recruitment via a IL-17A dependent pathway. The experimental aimed to explore the role of IL-17A in the gut microbiota-mediated enhancement of host resistance against systemic S. aureus infection. The experimental utilized WT mice assigned to No ABX, ABX, and FMT groups, as well as Il17a −/− mice assigned to No ABX and ABX groups. (A) WT mice were i.v . injected with S. aureus USA300, the level of IL-17A was determined in liver tissues by ELISA at 0, 6, 12, and 24 hours post-infection ( n = 5). (B-E) Hepatic IL-17A, KC, MIP-2, and MPO levels in No ABX, ABX, and FMT mice were measured by ELISA at 12 hours post-infection ( n = 5). (F) Schematic shows that Il17a −/− mice were pretreated with either No ABX or ABX containing water. Subsequently, along with the WT-No ABX group, all mice were challenged i.v . with S. aureus USA300. (G) Survival curves of WT-No ABX, Il17a −/− -No ABX, and Il17a −/− - ABX mice after i.v . challenged with S. aureus ( n = 10). (H) Bacterial burden in livers of WT-No ABX, Il17a −/− -No ABX, and Il17a −/− - ABX mice at 12 hours post-infection ( n = 7). (I) Representative contour plots of neutrophils (CD3 − CD11b + Ly6G + ) in liver at 12 hours post-infection. (J) Scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection. ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Article Snippet: A single dose of recombinant IL-17A (rIL-17A; MCE), at a dose of 1 μg per mouse based on previous studies [ , ], was dissolved in sterile PBS. rIL-17A or vehicle were mixed with the inoculum of S. aureus and administered intradermally to Tcrδ −/− mice.

    Techniques: Infection, Injection, Enzyme-linked Immunosorbent Assay

    Gut microbiota induces IL-17A production by hepatic γδ T cells to promote host systemic defense. The experimental aimed to identify the cellular sources of the key immune factor IL-17A in the liver during gut microbiota-mediated host defense against systemic S. aureus infection. The experimental utilized WT mice assigned to No ABX, ABX, and FMT groups, as well as Tcrδ −/− mice assigned to No ABX, ABX, and ABX+rIL-17A groups. (A) No ABX, ABX, and FMT mice were i.v . challenged with S. aureus USA300, and hepatic Th17 and γδT17 cell levels were measured at 12 hours post-infection. Representative contour plots of hepatic Th17 and γδT17 cells. (B) Scatter plots shown frequencies of hepatic Th17 and γδT17 cells ( n = 5). (C) Schematic shows that Tcrδ −/− mice were pretreated with either No ABX or ABX containing water, or administration with rIL-17A. Subsequently, along with the WT-No ABX group, all mice were challenged i.v . with S. aureus USA300. (D) The level of IL-17A + CD3 + cells in liver were measured in WT-No ABX, Tcrδ −/− -No ABX, and Tcrδ −/− -ABX mice at 12 hours post-infection ( n = 5). Representative contour plots of hepatic IL-17A + CD3 + cells. (E) Scatter plots shown frequencies of hepatic IL-17A + CD3 + cells. (F) ELSIA analyze level of IL-17A in liver. (G) Survival curves of WT-No ABX, Tcrδ −/− -No ABX, Tcrδ −/− -ABX, and Tcrδ −/− -ABX+rIL-17A mice after i.v . challenged with S. aureus ( n = 10). Statistical significance was determined by the log-rank (mantel-cox) test. (H) Bacterial burden in livers from WT-No ABX, Tcrδ −/− -No ABX, Tcrδ −/− -ABX, and Tcrδ −/− -ABX+rIL-17A mice at 12 hours post-infection ( n = 7). (I) Representative images of liver and kidney by H&E staining. Bar: 50 μm. (J) Representative contour plots of neutrophils in liver at 12 hours post-infection. (K) scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection. Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Journal: Virulence

    Article Title: Gut microbiota-driven IL-17A production by hepatic γδ T cells enhances neutrophil defense against systemic Staphylococcus aureus infection

    doi: 10.1080/21505594.2026.2629132

    Figure Lengend Snippet: Gut microbiota induces IL-17A production by hepatic γδ T cells to promote host systemic defense. The experimental aimed to identify the cellular sources of the key immune factor IL-17A in the liver during gut microbiota-mediated host defense against systemic S. aureus infection. The experimental utilized WT mice assigned to No ABX, ABX, and FMT groups, as well as Tcrδ −/− mice assigned to No ABX, ABX, and ABX+rIL-17A groups. (A) No ABX, ABX, and FMT mice were i.v . challenged with S. aureus USA300, and hepatic Th17 and γδT17 cell levels were measured at 12 hours post-infection. Representative contour plots of hepatic Th17 and γδT17 cells. (B) Scatter plots shown frequencies of hepatic Th17 and γδT17 cells ( n = 5). (C) Schematic shows that Tcrδ −/− mice were pretreated with either No ABX or ABX containing water, or administration with rIL-17A. Subsequently, along with the WT-No ABX group, all mice were challenged i.v . with S. aureus USA300. (D) The level of IL-17A + CD3 + cells in liver were measured in WT-No ABX, Tcrδ −/− -No ABX, and Tcrδ −/− -ABX mice at 12 hours post-infection ( n = 5). Representative contour plots of hepatic IL-17A + CD3 + cells. (E) Scatter plots shown frequencies of hepatic IL-17A + CD3 + cells. (F) ELSIA analyze level of IL-17A in liver. (G) Survival curves of WT-No ABX, Tcrδ −/− -No ABX, Tcrδ −/− -ABX, and Tcrδ −/− -ABX+rIL-17A mice after i.v . challenged with S. aureus ( n = 10). Statistical significance was determined by the log-rank (mantel-cox) test. (H) Bacterial burden in livers from WT-No ABX, Tcrδ −/− -No ABX, Tcrδ −/− -ABX, and Tcrδ −/− -ABX+rIL-17A mice at 12 hours post-infection ( n = 7). (I) Representative images of liver and kidney by H&E staining. Bar: 50 μm. (J) Representative contour plots of neutrophils in liver at 12 hours post-infection. (K) scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection. Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Article Snippet: A single dose of recombinant IL-17A (rIL-17A; MCE), at a dose of 1 μg per mouse based on previous studies [ , ], was dissolved in sterile PBS. rIL-17A or vehicle were mixed with the inoculum of S. aureus and administered intradermally to Tcrδ −/− mice.

    Techniques: Infection, Staining

    Gut microbiota induces IL-17A production by hepatic γδ T cells to promote host systemic defense. (A) The experimental aimed to determine the contribution of L. reuteri WX25, a specific commensal strain derived from the gut microbiota of healthy mice, to host protection against systemic S. aureus infection. The experimental design included the No ABX, Van+Amp, Van+Amp+FMT, and Van+Amp+ L. reuteri WX25 groups. Subsequently, all mice were challenged i.v . with S. aureus USA300. (B) Survival curves of No ABX, Van+Amp, FMT, L. reuteri WX25 mice after i.v . challenged with S. aureus ( n = 10). Statistical significance was determined by the log-rank (mantel-cox) test. (C) bacterial burden in livers from No ABX, Van+Amp, Van+Amp+FMT, and Van+Amp+ L. reuteri WX25 groups at 12 hours post-infection ( n = 6). (D) Representative images of liver and kidney by H&E staining at 12 hours post-infection. Bar: 50 μm. (E) Representative contour plots of γδT17 (CD3 + TCRγ/δ + IL-17A + ) cells in liver at 12 hours post-infection. (F) Scatter plots shown percentage of IL-17A + in γδ T cells in liver at 12 hours post-infection ( n = 5). (G) Representative contour plots of neutrophils in liver at 12 hours post-infection. (H) Scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Journal: Virulence

    Article Title: Gut microbiota-driven IL-17A production by hepatic γδ T cells enhances neutrophil defense against systemic Staphylococcus aureus infection

    doi: 10.1080/21505594.2026.2629132

    Figure Lengend Snippet: Gut microbiota induces IL-17A production by hepatic γδ T cells to promote host systemic defense. (A) The experimental aimed to determine the contribution of L. reuteri WX25, a specific commensal strain derived from the gut microbiota of healthy mice, to host protection against systemic S. aureus infection. The experimental design included the No ABX, Van+Amp, Van+Amp+FMT, and Van+Amp+ L. reuteri WX25 groups. Subsequently, all mice were challenged i.v . with S. aureus USA300. (B) Survival curves of No ABX, Van+Amp, FMT, L. reuteri WX25 mice after i.v . challenged with S. aureus ( n = 10). Statistical significance was determined by the log-rank (mantel-cox) test. (C) bacterial burden in livers from No ABX, Van+Amp, Van+Amp+FMT, and Van+Amp+ L. reuteri WX25 groups at 12 hours post-infection ( n = 6). (D) Representative images of liver and kidney by H&E staining at 12 hours post-infection. Bar: 50 μm. (E) Representative contour plots of γδT17 (CD3 + TCRγ/δ + IL-17A + ) cells in liver at 12 hours post-infection. (F) Scatter plots shown percentage of IL-17A + in γδ T cells in liver at 12 hours post-infection ( n = 5). (G) Representative contour plots of neutrophils in liver at 12 hours post-infection. (H) Scatter plots shown absolute number of neutrophils in liver at 12 hours post-infection ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Article Snippet: A single dose of recombinant IL-17A (rIL-17A; MCE), at a dose of 1 μg per mouse based on previous studies [ , ], was dissolved in sterile PBS. rIL-17A or vehicle were mixed with the inoculum of S. aureus and administered intradermally to Tcrδ −/− mice.

    Techniques: Derivative Assay, Infection, Staining

    Microbiota-derived indole metabolites promoted host defense against S. aureus systemic infection, involving the γδT17/neutrophil axis. (A) Commensal bacteria isolated from the mouse intestine showed colorimetric evidence of indole metabolites production, as determined by the Kovac’s reagent method. (B) Schematic illustration for the gut microbiota elimination and potential effector metabolites treatment. After antibiotic treatment, mice were treated with indole derivatives (IAld+IAA+IPA) by oral gavage ( i.g .) for 10 days. Subsequently, all mice were challenged i.v . with S. aureus USA300. (C) Survival curves of No ABX, Van+Amp, FMT, L. reuteri WX25 mice after i.v . challenged with S. aureus ( n = 10). Statistical significance was determined by the log-rank (mantel-cox) test. (D) Bacterial burden in livers from No ABX, Van+Amp, FMT, L. reuteri WX25 mice at 12 hours post-infection ( n = 5). (E-H) Hepatic IL-17A, MIP-2, KC, and MPO levels in WT-No ABX, WT-ABX, WT-Indoles, and Tcrδ −/− mice were measured by ELISA at 12 hours post-infection ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Journal: Virulence

    Article Title: Gut microbiota-driven IL-17A production by hepatic γδ T cells enhances neutrophil defense against systemic Staphylococcus aureus infection

    doi: 10.1080/21505594.2026.2629132

    Figure Lengend Snippet: Microbiota-derived indole metabolites promoted host defense against S. aureus systemic infection, involving the γδT17/neutrophil axis. (A) Commensal bacteria isolated from the mouse intestine showed colorimetric evidence of indole metabolites production, as determined by the Kovac’s reagent method. (B) Schematic illustration for the gut microbiota elimination and potential effector metabolites treatment. After antibiotic treatment, mice were treated with indole derivatives (IAld+IAA+IPA) by oral gavage ( i.g .) for 10 days. Subsequently, all mice were challenged i.v . with S. aureus USA300. (C) Survival curves of No ABX, Van+Amp, FMT, L. reuteri WX25 mice after i.v . challenged with S. aureus ( n = 10). Statistical significance was determined by the log-rank (mantel-cox) test. (D) Bacterial burden in livers from No ABX, Van+Amp, FMT, L. reuteri WX25 mice at 12 hours post-infection ( n = 5). (E-H) Hepatic IL-17A, MIP-2, KC, and MPO levels in WT-No ABX, WT-ABX, WT-Indoles, and Tcrδ −/− mice were measured by ELISA at 12 hours post-infection ( n = 5). Data are presented as means ± SD. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant; one-way ANOVA with Tukey’s for multiple comparisons.

    Article Snippet: A single dose of recombinant IL-17A (rIL-17A; MCE), at a dose of 1 μg per mouse based on previous studies [ , ], was dissolved in sterile PBS. rIL-17A or vehicle were mixed with the inoculum of S. aureus and administered intradermally to Tcrδ −/− mice.

    Techniques: Derivative Assay, Infection, Bacteria, Isolation, Enzyme-linked Immunosorbent Assay