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mouse il 25 elisa kit  (Multi Sciences (Lianke) Biotech Co Ltd)


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    Multi Sciences (Lianke) Biotech Co Ltd mouse il 25 elisa kit
    Mouse Il 25 Elisa Kit, supplied by Multi Sciences (Lianke) Biotech Co Ltd, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+il+25+elisa+kit/Mouse+IL-17E%2FIL-25+ELISA+Kit/pm39617924-213-15-19
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    Enzyme-linked Immunosorbent Assay:

    Article Title: Berberine ameliorates dextran sulfate sodium -induced colitis through tuft cells and bitter taste signalling.
    Article Snippet: Then they were centrifuged at 3000 g for 10 min and fixed in 1 mL PFA for 45 min. Staining was performed using anti-DCLK1/ MUC2/ChgA antibody, DAPI stain (Vazyme, Nanjing, China), following the aforementioned methods. .. The levels of IL-25 in the mouse colonic organoid culture supernatants were determined using a mouse IL-25 ELISA kit (MULTI SCIENCES, EK2179, Hangzhou, China). .. Colon tissues were homogenised in TRIzol before total RNA extraction using a RNA extraction kit (Thermo Fisher Scientific, Waltham, MA, USA), according to manufacturer’s instructions.

    Article Title: Berberine ameliorates dextran sulfate sodium -induced colitis through tuft cells and bitter taste signalling
    Article Snippet: Then they were centrifuged at 3000 g for 10 min and fixed in 1 mL PFA for 45 min. Staining was performed using anti-DCLK1/MUC2/ChgA antibody, DAPI stain (Vazyme, Nanjing, China), following the aforementioned methods. .. The levels of IL-25 in the mouse colonic organoid culture supernatants were determined using a mouse IL-25 ELISA kit (MULTI SCIENCES, EK2179, Hangzhou, China). .. Colon tissues were homogenised in TRIzol before total RNA extraction using a RNA extraction kit (Thermo Fisher Scientific, Waltham, MA, USA), according to manufacturer’s instructions.

    Article Title: Oral berberine ameliorates high-fat diet-induced obesity by activating TAS2Rs in tuft and endocrine cells in the gut.
    Article Snippet: Background and aims: Although oral berberine, a natural compound extracted from the Chinese herbal medicine curcumin, has low bioavailability, it is still effective in suppressing obesity; however, the underlying mechanism is unclear.. Berberine can bind to bitter-taste receptors (TAS2Rs) in intestinal endocrine secretin tumor (STC-1) cells to promote glucagon-like peptide-1 (GLP-1) secretion.. Notably, TAS2Rs also exist in the tuft cells of the gut.



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    Mouse Il 25 Elisa Kit, supplied by Multi Sciences (Lianke) Biotech Co Ltd, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    OTUD6A expression is upregulated in airway epithelial cells in asthma. A‐B) Immunohistochemical (IHC) staining and quantification of OTUD6A in human lung tissues from healthy controls ( n = 2) and asthmatic patients ( n = 2). Scale bars: 100 µm. C‐D) Western blot analysis of OTUD6A expression in lung tissue from HDM‐CAM (C) and HDM‐AAM (D) mice. E‐F) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐CAM and corresponding quantitative analysis ( n = 5). Scale bars: 100 µm. G‐H) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars; 100 µm. I‐J) Immunofluorescence staining for OTUD6A in the mouse lung tissue of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars: 50 µm. K) Western blot analysis of OTUD6A protein levels in BEAS‐2B cells stimulated with HDM (100 µg/mL) at indicated time points ( n = 5). L‐M) BEAS‐2B cells transfected with OTUD6A or control vector for 24 h. L) Western blot analysis of ZO‐1 and Occludin. M) RT‐qPCR analysis <t>of</t> <t>IL‐25</t> , IL‐33 , and TSLP mRNA levels ( n = 5). N‐O) HBEpiC cells transfected with OTUD6A or control vector for 24 h. N) Western blot analysis of ZO‐1 and Occludin. O) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). P‐Q) HBEpiC cells transfected with siOTUD6A or control vector for 48 h and stimulated with HDM (100 µg/mL) for 6 h. P) Western blot analysis of OTUD6A, ZO‐1, and Occludin. Q) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). Data are presented as mean ± SEM. P values determined by two‐tailed unpaired t‐test or one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).
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    OTUD6A expression is upregulated in airway epithelial cells in asthma. A‐B) Immunohistochemical (IHC) staining and quantification of OTUD6A in human lung tissues from healthy controls ( n = 2) and asthmatic patients ( n = 2). Scale bars: 100 µm. C‐D) Western blot analysis of OTUD6A expression in lung tissue from HDM‐CAM (C) and HDM‐AAM (D) mice. E‐F) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐CAM and corresponding quantitative analysis ( n = 5). Scale bars: 100 µm. G‐H) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars; 100 µm. I‐J) Immunofluorescence staining for OTUD6A in the mouse lung tissue of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars: 50 µm. K) Western blot analysis of OTUD6A protein levels in BEAS‐2B cells stimulated with HDM (100 µg/mL) at indicated time points ( n = 5). L‐M) BEAS‐2B cells transfected with OTUD6A or control vector for 24 h. L) Western blot analysis of ZO‐1 and Occludin. M) RT‐qPCR analysis <t>of</t> <t>IL‐25</t> , IL‐33 , and TSLP mRNA levels ( n = 5). N‐O) HBEpiC cells transfected with OTUD6A or control vector for 24 h. N) Western blot analysis of ZO‐1 and Occludin. O) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). P‐Q) HBEpiC cells transfected with siOTUD6A or control vector for 48 h and stimulated with HDM (100 µg/mL) for 6 h. P) Western blot analysis of OTUD6A, ZO‐1, and Occludin. Q) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). Data are presented as mean ± SEM. P values determined by two‐tailed unpaired t‐test or one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).
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    <t>IL-25</t> <t>expression</t> peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    <t>IL-25</t> <t>expression</t> peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    <t>IL-25</t> <t>expression</t> peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    <t>IL-25</t> <t>expression</t> peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    <t>IL-25</t> <t>expression</t> peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001
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    OTUD6A expression is upregulated in airway epithelial cells in asthma. A‐B) Immunohistochemical (IHC) staining and quantification of OTUD6A in human lung tissues from healthy controls ( n = 2) and asthmatic patients ( n = 2). Scale bars: 100 µm. C‐D) Western blot analysis of OTUD6A expression in lung tissue from HDM‐CAM (C) and HDM‐AAM (D) mice. E‐F) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐CAM and corresponding quantitative analysis ( n = 5). Scale bars: 100 µm. G‐H) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars; 100 µm. I‐J) Immunofluorescence staining for OTUD6A in the mouse lung tissue of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars: 50 µm. K) Western blot analysis of OTUD6A protein levels in BEAS‐2B cells stimulated with HDM (100 µg/mL) at indicated time points ( n = 5). L‐M) BEAS‐2B cells transfected with OTUD6A or control vector for 24 h. L) Western blot analysis of ZO‐1 and Occludin. M) RT‐qPCR analysis of IL‐25 , IL‐33 , and TSLP mRNA levels ( n = 5). N‐O) HBEpiC cells transfected with OTUD6A or control vector for 24 h. N) Western blot analysis of ZO‐1 and Occludin. O) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). P‐Q) HBEpiC cells transfected with siOTUD6A or control vector for 48 h and stimulated with HDM (100 µg/mL) for 6 h. P) Western blot analysis of OTUD6A, ZO‐1, and Occludin. Q) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). Data are presented as mean ± SEM. P values determined by two‐tailed unpaired t‐test or one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Advanced Science

    Article Title: OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

    doi: 10.1002/advs.202516355

    Figure Lengend Snippet: OTUD6A expression is upregulated in airway epithelial cells in asthma. A‐B) Immunohistochemical (IHC) staining and quantification of OTUD6A in human lung tissues from healthy controls ( n = 2) and asthmatic patients ( n = 2). Scale bars: 100 µm. C‐D) Western blot analysis of OTUD6A expression in lung tissue from HDM‐CAM (C) and HDM‐AAM (D) mice. E‐F) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐CAM and corresponding quantitative analysis ( n = 5). Scale bars: 100 µm. G‐H) Representative images of IHC for OTUD6A on mouse lung sections of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars; 100 µm. I‐J) Immunofluorescence staining for OTUD6A in the mouse lung tissue of HDM‐AAM and corresponding quantitative analysis ( n = 5). Scale bars: 50 µm. K) Western blot analysis of OTUD6A protein levels in BEAS‐2B cells stimulated with HDM (100 µg/mL) at indicated time points ( n = 5). L‐M) BEAS‐2B cells transfected with OTUD6A or control vector for 24 h. L) Western blot analysis of ZO‐1 and Occludin. M) RT‐qPCR analysis of IL‐25 , IL‐33 , and TSLP mRNA levels ( n = 5). N‐O) HBEpiC cells transfected with OTUD6A or control vector for 24 h. N) Western blot analysis of ZO‐1 and Occludin. O) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). P‐Q) HBEpiC cells transfected with siOTUD6A or control vector for 48 h and stimulated with HDM (100 µg/mL) for 6 h. P) Western blot analysis of OTUD6A, ZO‐1, and Occludin. Q) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). Data are presented as mean ± SEM. P values determined by two‐tailed unpaired t‐test or one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Human IL‐25 (Cat# E‐EL‐H1648)/IL‐33 (E‐EL‐H2402)/TSLP (Cat# E‐EL‐H1598)/Resistin (Cat# E‐EL‐H1213) ELISA kits, and mouse IL‐25 (Cat# E‐EL‐M0187)/IL‐33 (Cat# E‐EL‐M2642)/TSLP (Cat# E‐EL‐M0642) ELISA kits were purchased from Elabscience (Wuhan, China).

    Techniques: Expressing, Immunohistochemical staining, Immunohistochemistry, Western Blot, Immunofluorescence, Staining, Transfection, Control, Plasmid Preparation, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Two Tailed Test

    OTUD6A knockout alleviates asthma in HDM‐induced acute asthma model. A) Schematic diagram depicting the procedure of HDM‐AAM. B) AHR assessed via acetylcholine challenge ( n = 5). C) Serum IgE levels measured by ELISA ( n = 5). D) Representative H&E and PAS staining of lung tissue. Scale bars: 100 µm. E) Quantification of bronchial epithelial thickness ( n = 5). F) BALF eosinophil counts determined by Wright‐Giemsa staining ( n = 5). G‐J) IL‐5 and IL‐13 levels in BALF (G, H) and lung homogenates (I, J) measured by ELISA ( n = 5). K‐N) RT‐qPCR analysis of Il5 , Il13 , Muc5ac , and Muc5b mRNA levels in lung tissue ( n = 5). O) ELISA analysis of IL‐25, IL‐33, and TSLP levels in BALF ( n = 5). P) Western blot and quantification of ZO‐1 and Occludin in lung tissues. Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Advanced Science

    Article Title: OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

    doi: 10.1002/advs.202516355

    Figure Lengend Snippet: OTUD6A knockout alleviates asthma in HDM‐induced acute asthma model. A) Schematic diagram depicting the procedure of HDM‐AAM. B) AHR assessed via acetylcholine challenge ( n = 5). C) Serum IgE levels measured by ELISA ( n = 5). D) Representative H&E and PAS staining of lung tissue. Scale bars: 100 µm. E) Quantification of bronchial epithelial thickness ( n = 5). F) BALF eosinophil counts determined by Wright‐Giemsa staining ( n = 5). G‐J) IL‐5 and IL‐13 levels in BALF (G, H) and lung homogenates (I, J) measured by ELISA ( n = 5). K‐N) RT‐qPCR analysis of Il5 , Il13 , Muc5ac , and Muc5b mRNA levels in lung tissue ( n = 5). O) ELISA analysis of IL‐25, IL‐33, and TSLP levels in BALF ( n = 5). P) Western blot and quantification of ZO‐1 and Occludin in lung tissues. Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Human IL‐25 (Cat# E‐EL‐H1648)/IL‐33 (E‐EL‐H2402)/TSLP (Cat# E‐EL‐H1598)/Resistin (Cat# E‐EL‐H1213) ELISA kits, and mouse IL‐25 (Cat# E‐EL‐M0187)/IL‐33 (Cat# E‐EL‐M2642)/TSLP (Cat# E‐EL‐M0642) ELISA kits were purchased from Elabscience (Wuhan, China).

    Techniques: Knock-Out, Enzyme-linked Immunosorbent Assay, Staining, Quantitative RT-PCR, Western Blot

    OTUD6A knockout mitigates asthma in HDM‐induced chronic asthma model. A) Schematic diagram depicting the procedure of HDM‐CAM. B‐D) Rn, Ers, and Rrs assessed via methacholine challenge ( n = 5). E) Representative H&E staining of lung tissue. Scale bars: 100 µm. F) Serum IgE levels measured by ELISA ( n = 5). G‐H) Total cell counts (G) and protein concentration (H) in BALF ( n = 5). I‐L) IL‐5 and IL‐13 levels in BALF (I, J) and lung homogenates (K, L) measured by ELISA ( n = 5). M‐R) RT‐qPCR analysis of Il5 , Il13 , Muc5ac , Tslp , Il25 , and Il33 mRNA level in lung tissues ( n = 5). S‐U) ELISA analysis of IL‐25, IL‐33, and TSLP levels in BALF ( n = 5). Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Advanced Science

    Article Title: OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

    doi: 10.1002/advs.202516355

    Figure Lengend Snippet: OTUD6A knockout mitigates asthma in HDM‐induced chronic asthma model. A) Schematic diagram depicting the procedure of HDM‐CAM. B‐D) Rn, Ers, and Rrs assessed via methacholine challenge ( n = 5). E) Representative H&E staining of lung tissue. Scale bars: 100 µm. F) Serum IgE levels measured by ELISA ( n = 5). G‐H) Total cell counts (G) and protein concentration (H) in BALF ( n = 5). I‐L) IL‐5 and IL‐13 levels in BALF (I, J) and lung homogenates (K, L) measured by ELISA ( n = 5). M‐R) RT‐qPCR analysis of Il5 , Il13 , Muc5ac , Tslp , Il25 , and Il33 mRNA level in lung tissues ( n = 5). S‐U) ELISA analysis of IL‐25, IL‐33, and TSLP levels in BALF ( n = 5). Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Human IL‐25 (Cat# E‐EL‐H1648)/IL‐33 (E‐EL‐H2402)/TSLP (Cat# E‐EL‐H1598)/Resistin (Cat# E‐EL‐H1213) ELISA kits, and mouse IL‐25 (Cat# E‐EL‐M0187)/IL‐33 (Cat# E‐EL‐M2642)/TSLP (Cat# E‐EL‐M0642) ELISA kits were purchased from Elabscience (Wuhan, China).

    Techniques: Knock-Out, Staining, Enzyme-linked Immunosorbent Assay, Protein Concentration, Quantitative RT-PCR

    hResistin/PI3K mediates OTUD6A‐induced EMT process and the expression of epithelial‐derived alarmins. A‐G) BEAS‐2B cells transfected with siResistin for 48 h and then transfected with Flag‐OTUD6A for 24 h. A) RT‐qPCR analysis of TSLP , IL‐25 , IL‐33 mRNA level in BEAS‐2B cells ( n = 5). B) ELISA analysis of TSLP, IL‐25, and IL‐33 levels in cell supernatant ( n = 5). C) RT‐qPCR analysis of TGFB1 , ACTA2 , COL1A1 mRNA level in BEAS‐2B cells ( n = 5). D‐E) Western blot analysis of OTUD6A, hResistin, EMT, and PI3K/AKT markers. F) Immunofluorescence staining of E‐cadherin and N‐cadherin. Scale bars: 50 µm. G) Cell wound healing assay. Scale bars: 50 µm. H‐K) BEAS‐2B cells were pretreated with LY294002 (30 µ m ) for 30 min and transfected with Flag‐OTUD6A for 24 h. H) Western blot analysis of hResistin and EMT markers. I‐K) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Advanced Science

    Article Title: OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

    doi: 10.1002/advs.202516355

    Figure Lengend Snippet: hResistin/PI3K mediates OTUD6A‐induced EMT process and the expression of epithelial‐derived alarmins. A‐G) BEAS‐2B cells transfected with siResistin for 48 h and then transfected with Flag‐OTUD6A for 24 h. A) RT‐qPCR analysis of TSLP , IL‐25 , IL‐33 mRNA level in BEAS‐2B cells ( n = 5). B) ELISA analysis of TSLP, IL‐25, and IL‐33 levels in cell supernatant ( n = 5). C) RT‐qPCR analysis of TGFB1 , ACTA2 , COL1A1 mRNA level in BEAS‐2B cells ( n = 5). D‐E) Western blot analysis of OTUD6A, hResistin, EMT, and PI3K/AKT markers. F) Immunofluorescence staining of E‐cadherin and N‐cadherin. Scale bars: 50 µm. G) Cell wound healing assay. Scale bars: 50 µm. H‐K) BEAS‐2B cells were pretreated with LY294002 (30 µ m ) for 30 min and transfected with Flag‐OTUD6A for 24 h. H) Western blot analysis of hResistin and EMT markers. I‐K) ELISA analysis of IL‐33, IL‐25, and TSLP levels in cell supernatant ( n = 5). Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Human IL‐25 (Cat# E‐EL‐H1648)/IL‐33 (E‐EL‐H2402)/TSLP (Cat# E‐EL‐H1598)/Resistin (Cat# E‐EL‐H1213) ELISA kits, and mouse IL‐25 (Cat# E‐EL‐M0187)/IL‐33 (Cat# E‐EL‐M2642)/TSLP (Cat# E‐EL‐M0642) ELISA kits were purchased from Elabscience (Wuhan, China).

    Techniques: Expressing, Derivative Assay, Transfection, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Western Blot, Immunofluorescence, Staining, Wound Healing Assay

    Lung‐specific OTUD6A knockdown attenuates HDM‐induced asthma. A) Schematic diagram depicting the procedure of HDM‐induced chronic asthma model. B) Western blot analysis of OTUD6A and mRELMα in lung tissues. C) AHR assessed via acetylcholine challenge ( n = 5). D) H&E staining of lung tissues. Scale bars: 100 µm. E) Serum IgE levels measured by ELISA ( n = 5). F‐G) Total cell counts (F) and protein concentration (G) in BALF ( n = 5). H‐I) IL‐5 (H) and IL‐13 (I) levels in BALF measured by ELISA ( n = 5). J‐L) RT‐qPCR analysis of Il4, Il5 , and Muc5ac mRNA levels in lung tissues ( n = 5). M) ELISA analysis of IL‐25, IL‐33, and TSLP levels in BALF (n = 5). N) Serum TGF‐β1 levels measured by ELISA ( n = 5). O) Masson's trichrome staining of lung sections. Scale bars: 100 µm. P) RT‐qPCR analysis of Tgfb1 , Acta2 , and Col1a1 mRNA levels in lung tissues ( n = 5). Q) Western blot analysis of Vimentin, TGFβ1, α‐SMA, and Fibronectin in the lung tissues. R) Western blot analysis of PI3K/AKT in the lung tissues. S) Western blot analysis of EMT markers in the lung tissues. Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Advanced Science

    Article Title: OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα

    doi: 10.1002/advs.202516355

    Figure Lengend Snippet: Lung‐specific OTUD6A knockdown attenuates HDM‐induced asthma. A) Schematic diagram depicting the procedure of HDM‐induced chronic asthma model. B) Western blot analysis of OTUD6A and mRELMα in lung tissues. C) AHR assessed via acetylcholine challenge ( n = 5). D) H&E staining of lung tissues. Scale bars: 100 µm. E) Serum IgE levels measured by ELISA ( n = 5). F‐G) Total cell counts (F) and protein concentration (G) in BALF ( n = 5). H‐I) IL‐5 (H) and IL‐13 (I) levels in BALF measured by ELISA ( n = 5). J‐L) RT‐qPCR analysis of Il4, Il5 , and Muc5ac mRNA levels in lung tissues ( n = 5). M) ELISA analysis of IL‐25, IL‐33, and TSLP levels in BALF (n = 5). N) Serum TGF‐β1 levels measured by ELISA ( n = 5). O) Masson's trichrome staining of lung sections. Scale bars: 100 µm. P) RT‐qPCR analysis of Tgfb1 , Acta2 , and Col1a1 mRNA levels in lung tissues ( n = 5). Q) Western blot analysis of Vimentin, TGFβ1, α‐SMA, and Fibronectin in the lung tissues. R) Western blot analysis of PI3K/AKT in the lung tissues. S) Western blot analysis of EMT markers in the lung tissues. Data are presented as mean ± SEM. P values determined by one‐way ANOVA (* p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Human IL‐25 (Cat# E‐EL‐H1648)/IL‐33 (E‐EL‐H2402)/TSLP (Cat# E‐EL‐H1598)/Resistin (Cat# E‐EL‐H1213) ELISA kits, and mouse IL‐25 (Cat# E‐EL‐M0187)/IL‐33 (Cat# E‐EL‐M2642)/TSLP (Cat# E‐EL‐M0642) ELISA kits were purchased from Elabscience (Wuhan, China).

    Techniques: Knockdown, Western Blot, Staining, Enzyme-linked Immunosorbent Assay, Protein Concentration, Quantitative RT-PCR

    IL-25 expression peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-25 expression peaked at day 3 after TBI and predominantly localized to neuron and BMECs. A Temporal profile of IL-25 expression in a murine TBI model. B - C IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( B ) and serum ( C ) of mice (n = 6 per group). D Schematic workflow of TBI modeling and therapeutic administration in mice. E - F IL-25 cytokine levels in ipsilateral cerebral cortex tissue ( E ) and serum ( F ) of mice at 3 days after TBI (n = 6 per group). G Representative immunofluorescence images showing IL-25 (green) co-stained with NeuN (neuron), CD31 (endothelial cells), GFAP (astrocytes), or Iba-1 (microglia) (red) in the ipsilateral cortex 3 days after TBI and co-localization ratio (Pearsons) (n = 6 per group). Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. Data presentation: Mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques: Expressing, Immunofluorescence, Staining

    IL-25 administration restores BBB integrity following TBI. A - D Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( A ), ZO-1 quantification ( B ), Occludin quantification ( C ), Claudin-5 quantification ( D ) ( n = 6 per group). E Immunofluorescence of ZO-1 (red) co-stained with CD31 (endothelial cells) (green) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. F Immunofluorescence of TUNEL (green) co-stained with CD31 (endothelial cells) (red) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm. G Quantification of endothelial expression of ZO-1 in the ipsilateral cortex 3 days after TBI ( n = 6 per group). H Quantification of endothelial expression of TUNEL in the ipsilateral cortex 3 days after TBI ( n = 6 per group). I Representative macroscopic images of Evans Blue extravasation (blue areas) in brain tissue 3 days after TBI. J Quantitative analysis of Evans Blue leakage in ipsilateral hemispheres ( n = 6 per group). K The brain water content of mice 3 days after TBI ( n = 6 per group). L Representative T2-weighted MRI of whole brains 3 days after TBI. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-25 administration restores BBB integrity following TBI. A - D Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( A ), ZO-1 quantification ( B ), Occludin quantification ( C ), Claudin-5 quantification ( D ) ( n = 6 per group). E Immunofluorescence of ZO-1 (red) co-stained with CD31 (endothelial cells) (green) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 50 μm. F Immunofluorescence of TUNEL (green) co-stained with CD31 (endothelial cells) (red) in the ipsilateral cortex 3 days after TBI. Nuclei were counterstained with DAPI (blue). Scale bar = 20 μm. G Quantification of endothelial expression of ZO-1 in the ipsilateral cortex 3 days after TBI ( n = 6 per group). H Quantification of endothelial expression of TUNEL in the ipsilateral cortex 3 days after TBI ( n = 6 per group). I Representative macroscopic images of Evans Blue extravasation (blue areas) in brain tissue 3 days after TBI. J Quantitative analysis of Evans Blue leakage in ipsilateral hemispheres ( n = 6 per group). K The brain water content of mice 3 days after TBI ( n = 6 per group). L Representative T2-weighted MRI of whole brains 3 days after TBI. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques: Western Blot, Immunofluorescence, Staining, TUNEL Assay, Expressing

    IL-25 improves neurological recovery after TBI. A Schematic workflow of TBI modeling, therapeutic administration, and behavioral assessment timeline. B - C Longitudinal assessment of sensorimotor function: mNSS ( B ), Latency to fall on accelerating rotarod ( C ) ( n = 6 per group). D - G Morris Water Maze cognitive evaluation after TBI: Representative swim paths ( D ), Escape latency during acquisition trials (days 1–5) ( E ), Platform crossings during probe trial (days 6) ( F ), Time spent in target quadrant during probe trial (days 6) ( G ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; when the TBI + PBS group was compared to the Sham group, # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001, when the TBI + IL-25 group was compared to the TBI + PBS group, * p < 0.05, ** p < 0.01, ** p < 0.01, *** p < 0.001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-25 improves neurological recovery after TBI. A Schematic workflow of TBI modeling, therapeutic administration, and behavioral assessment timeline. B - C Longitudinal assessment of sensorimotor function: mNSS ( B ), Latency to fall on accelerating rotarod ( C ) ( n = 6 per group). D - G Morris Water Maze cognitive evaluation after TBI: Representative swim paths ( D ), Escape latency during acquisition trials (days 1–5) ( E ), Platform crossings during probe trial (days 6) ( F ), Time spent in target quadrant during probe trial (days 6) ( G ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; when the TBI + PBS group was compared to the Sham group, # p < 0.05, ## p < 0.01, ### p < 0.001, #### p < 0.0001, when the TBI + IL-25 group was compared to the TBI + PBS group, * p < 0.05, ** p < 0.01, ** p < 0.01, *** p < 0.001

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques:

    IL-25 activates ILC2s and stimulates the production of downstream factors IL-5/IL-13. A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-25 activates ILC2s and stimulates the production of downstream factors IL-5/IL-13. A Single-Cell transcriptomic atlas of after TBI mice brain UMAP projection of 29,046 single cells isolated from cerebral cortex tissues of Sham (7,963), TBI + PBS (9,332 ), and TBI + IL-25 (11,751) groups. Colors represent distinct cell populations identified through unsupervised clustering. B Proportions of BBB-associated cells (endothelial cells, astrocytes, pericytes) across Sham, TBI + PBS, and TBI + IL-25 groups. C Heatmap visualization of differentially expressed genes in endothelial cells isolated from Sham, TBI + PBS, and TBI + IL-25 treatment groups. D KEGG network pathway enrichment analysis of differentially expressed genes in endothelial cells from the SHAM, TBI + PBS, and TBI + IL-25 groups. E Integrated KEGG pathway analysis of the three groups. F Cell-cell communication analysis depicting differential gene expression between endothelial cells and ILC2s. G Flow cytometry gating strategy for ILC2 identification: lymphocytes were selected by FSC/SSC, followed by detection of Lin - CD45 + CD127 + ST2 + cells. H - I Representative flow plots ( H ) and quantitative analysis ( I ) of cerebral cortex ILC2s at 3 days after TBI ( n = 3 per group). J - M Cytokine levels in ipsilateral cerebral cortex tissue and serum at 3 days after TBI: IL-5 (cerebral cortex) ( J ), IL-5 (serum) ( K ), IL-13 (cerebral cortex) ( L ), IL-13 (serum) ( M ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques: Single Cell, Isolation, Gene Expression, Flow Cytometry

    IL-13 preserves BBB integrity and attenuates pyroptosis in bEnd.3 cells after OGD/R injury. A Experimental workflow of OGD/R modeling and treatment in bEnd.3 cells. (B-C) IL-5 ( B ) and IL-13 ( C ) levels in supernatants of bEnd.3 cells after OGD/R ± IL-25 treatment (n = 6 per group). D - H Western blot analysis of bEnd.3 cells after OGD/R with or without IL-25, IL-5, or IL-13 treatment: Representative blots ( D ), ZO-1 quantification ( E ), Occludin quantification ( F ), Claudin-5 quantification ( G ), Caspase-1 quantification ( H ) (n = 6 per group). I - J Representative flow cytometry plots ( I ) and quantitative analysis ( J ) of apoptosis in bEnd.3 cells subjected to OGD/R with or without IL-25, IL-5, or IL-13 treatment (n = 6 per group). Viable cells: Annexin V⁻/PI⁻; Early apoptotic: Annexin V⁺/PI⁻; Late apoptotic: Annexin V⁺/PI⁺. K Immunofluorescence of ZO-1 and Claudin-5 (green) in bEnd.3 cells monolayers after OGD/R ± IL-13 treatment. Nuclei counterstained with DAPI (blue). Scale bar = 100 μm. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-13 preserves BBB integrity and attenuates pyroptosis in bEnd.3 cells after OGD/R injury. A Experimental workflow of OGD/R modeling and treatment in bEnd.3 cells. (B-C) IL-5 ( B ) and IL-13 ( C ) levels in supernatants of bEnd.3 cells after OGD/R ± IL-25 treatment (n = 6 per group). D - H Western blot analysis of bEnd.3 cells after OGD/R with or without IL-25, IL-5, or IL-13 treatment: Representative blots ( D ), ZO-1 quantification ( E ), Occludin quantification ( F ), Claudin-5 quantification ( G ), Caspase-1 quantification ( H ) (n = 6 per group). I - J Representative flow cytometry plots ( I ) and quantitative analysis ( J ) of apoptosis in bEnd.3 cells subjected to OGD/R with or without IL-25, IL-5, or IL-13 treatment (n = 6 per group). Viable cells: Annexin V⁻/PI⁻; Early apoptotic: Annexin V⁺/PI⁻; Late apoptotic: Annexin V⁺/PI⁺. K Immunofluorescence of ZO-1 and Claudin-5 (green) in bEnd.3 cells monolayers after OGD/R ± IL-13 treatment. Nuclei counterstained with DAPI (blue). Scale bar = 100 μm. Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques: Western Blot, Flow Cytometry, Immunofluorescence

    IL-13 improves BBB function by reducing CXCL-10 expression. A - B Cytokine array analysis identified CXCL-10 as one of the significantly downregulated cytokines in the IL-13-treated groups ( n = 3 per group). C - D CXCL-10 expression in bEnd.3 cells subjected to OGD/R ± IL-25, IL-5, or IL-13: Representative Western blot ( C ) and quantification ( D ) ( n = 6 per group). E - F CXCL-10 levels in ipsilateral cortex 3 days after TBI: Representative blot ( E ) and quantification ( F ) ( n = 6 per group). G Experimental workflow of TBI modeling and therapeutic administration. H - K Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( H ), ZO-1 quantification ( I ), Occludin quantification ( J ), Claudin-5 quantification ( K ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: IL-13 improves BBB function by reducing CXCL-10 expression. A - B Cytokine array analysis identified CXCL-10 as one of the significantly downregulated cytokines in the IL-13-treated groups ( n = 3 per group). C - D CXCL-10 expression in bEnd.3 cells subjected to OGD/R ± IL-25, IL-5, or IL-13: Representative Western blot ( C ) and quantification ( D ) ( n = 6 per group). E - F CXCL-10 levels in ipsilateral cortex 3 days after TBI: Representative blot ( E ) and quantification ( F ) ( n = 6 per group). G Experimental workflow of TBI modeling and therapeutic administration. H - K Western blot analysis of TJs (ZO-1, Occludin, Claudin-5) in the ipsilateral cortex 3 days after TBI: Representative blots ( H ), ZO-1 quantification ( I ), Occludin quantification ( J ), Claudin-5 quantification ( K ) ( n = 6 per group). Data presented as mean ± SD; ns: not significant; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques: Expressing, Western Blot

    Graphical abstract: IL-25-activated ILC2s secrete IL-13 to improve BBB function after TBI, by Figdraw

    Journal: Journal of Neuroinflammation

    Article Title: IL-25–ILC2–IL-13 axis improves traumatic brain injury by mediating CXCL-10-dependent regulation of blood brain barrier integrity

    doi: 10.1186/s12974-026-03696-4

    Figure Lengend Snippet: Graphical abstract: IL-25-activated ILC2s secrete IL-13 to improve BBB function after TBI, by Figdraw

    Article Snippet: Plasma and cerebral cortex tissue concentrations of IL-25, IL-5, and IL-13 were quantified after injury using commercial ELISA kits according to the manufacturers’ instructions: Mouse IL-25 ELISA Kit (RK00047, ABclonal, China), Mouse IL-5 ELISA Kit (HJ181, Epizyme Biotech, USA), and Mouse IL-13 ELISA Kit (HJ254, Epizyme Biotech, USA).

    Techniques: