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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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1) Product Images from "OTUD6A in Airway Epithelial Cells Exacerbates Allergic Asthma by Promoting Airway Inflammation and Airway Remodeling Through Deubiquitination of hResistin/mRELMα"

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

Journal: Advanced Science

doi: 10.1002/advs.202516355

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

Techniques Used: 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).

Figure Legend 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).

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

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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

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).

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

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).

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

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).

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

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).

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

a Immunofluorescent staining and quantification of IGF1⁺ epithelial cells at bronchial mucosae from control ( n = 6), SEA ( n = 9), EGPA ( n = 10), Cs-remission ( n = 3), and Cs-relapse ( n = 5) groups (biological replicates). Scale bar: 100 μm. b Bar plots of IGF1 concentrations in sputum samples from Control ( n = 13), SEA ( n = 23), and EGPA ( n = 21) (biological replicates). c Schematic of EGPA airway epithelial cells in ALI culture stimulated with IL-13, IL-33, or medium (Control). Bar plots show relative expression of IGF1 , IGF1R , and IGFBP3 , and IGF1 concentrations under different conditions. Data from 3 independent experiments (biological replicates). d Schematic of ALI system with IGF1 stimulation versus control. Representative histological (HE, PAS) and immunofluorescent (MUC5AC with DAPI) staining demonstrate morphological changes and mucin production (goblet hyperplasia) in ALI cultures with medium (Control) or IGF1 stimulation. Scale bars: 50 μm (HE, PAS), 20 μm (MUC5AC). Bar plots of IL-25, IL-33, and TSLP concentrations in culture supernatant at time points (Day 9, 13, 17, 21). Data from 3 independent experiments (biological replicates). e Scatter plot showing positive correlation between eosinophil abundance and IGF1 concentration in sputum from EGPA patients ( n = 21). f Schematic of proposed mechanism where IGF1 promotes goblet hyperplasia and augments T2-mediated inflammation through IGF1-IL25 loop, contributing to disease exacerbation in asthma and EGPA. Data presented as mean ± SD. a – c Two-sided one-way ANOVA with Tukey’s post-hoc test. d Two-sided unpaired t -test. e Two-sided Pearson correlation test. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . ALI air-liquid interface, HE hematoxylin and eosin, IGF1R insulin-like growth factor 1 receptor, IGFBP3 insulin-like growth factor binding protein 3, PAS periodic acid-Schiff, TSLP thymic stromal lymphopoietin.

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a Immunofluorescent staining and quantification of IGF1⁺ epithelial cells at bronchial mucosae from control ( n = 6), SEA ( n = 9), EGPA ( n = 10), Cs-remission ( n = 3), and Cs-relapse ( n = 5) groups (biological replicates). Scale bar: 100 μm. b Bar plots of IGF1 concentrations in sputum samples from Control ( n = 13), SEA ( n = 23), and EGPA ( n = 21) (biological replicates). c Schematic of EGPA airway epithelial cells in ALI culture stimulated with IL-13, IL-33, or medium (Control). Bar plots show relative expression of IGF1 , IGF1R , and IGFBP3 , and IGF1 concentrations under different conditions. Data from 3 independent experiments (biological replicates). d Schematic of ALI system with IGF1 stimulation versus control. Representative histological (HE, PAS) and immunofluorescent (MUC5AC with DAPI) staining demonstrate morphological changes and mucin production (goblet hyperplasia) in ALI cultures with medium (Control) or IGF1 stimulation. Scale bars: 50 μm (HE, PAS), 20 μm (MUC5AC). Bar plots of IL-25, IL-33, and TSLP concentrations in culture supernatant at time points (Day 9, 13, 17, 21). Data from 3 independent experiments (biological replicates). e Scatter plot showing positive correlation between eosinophil abundance and IGF1 concentration in sputum from EGPA patients ( n = 21). f Schematic of proposed mechanism where IGF1 promotes goblet hyperplasia and augments T2-mediated inflammation through IGF1-IL25 loop, contributing to disease exacerbation in asthma and EGPA. Data presented as mean ± SD. a – c Two-sided one-way ANOVA with Tukey’s post-hoc test. d Two-sided unpaired t -test. e Two-sided Pearson correlation test. * P < 0.05, ** P < 0.01, *** P < 0.001; NS, not significant. Exact P values in Supplementary Data . ALI air-liquid interface, HE hematoxylin and eosin, IGF1R insulin-like growth factor 1 receptor, IGFBP3 insulin-like growth factor binding protein 3, PAS periodic acid-Schiff, TSLP thymic stromal lymphopoietin.

Article Snippet: Mice were administered 50 μg of low-endotoxin HDM (Greer Labs, Cat# XPB91D3A2.5) combined with 500 ng recombinant mouse IL-33 (PEPROTECH, Cat# 210-33) via intranasal injection (i.n.) at Day 0, Day 7, Day 14 and Day 21, and recombinant IL−25 (2 μg in 50 μL saline, recombinant mouse IL25, R&D System, Cat# 1399-IL-025) was administered via intranasal injection (i.n.) at Day 15, Day 17, Day 19, and Day 21, Mice were sacrificed at Day 24, and tissues were harvested for downstream analysis.

Techniques: Staining, Control, Expressing, Concentration Assay, Binding Assay

a – e Anti-IGF1 treatment reduces eosinophilic inflammation and airway remodeling in IL-5 transgenic mice challenged with HDM and IL-33. Mice were divided into Control (PBS-treated), Model (HDM+IL-33 challenged), and Anti-IGF1 (HDM+IL-33+anti-IGF1 antibody) groups. a Total cell counts in bronchoalveolar lavage fluid (BALF) from control, model, and anti-IGF1-treated groups. b Eosinophil percentage in BALF. c Absolute eosinophil counts in BALF. d IL−25 levels in BALF quantified by ELISA. e Representative histological images of lung sections stained with hematoxylin and eosin (H&E, upper panels) and periodic acid-Schiff (PAS, lower panels), with corresponding inflammation and PAS score quantifications. Scale bar, 100 μm. f – h IGF1R deficiency modulates eosinophilic inflammation and airway remodeling via IL−25 in HDM+IL-33 challenged mice. f Total cell counts in BALF from wild-type (WT, Scgb1a1 -IRES-+/+ Igf1r f/f ), conditional knockout ( Scgb1a1 -IRES-Cre/+ Igf1r f/f , CKO), and CKO mice treated with recombinant IL-25 (rIL-25). All groups were challenged with HDM+IL-33. g Flow cytometric analysis of eosinophils (CD45 + Siglec-F + CD11c - ) in BALF. Representative plots and quantification of eosinophil percentages are shown. h Representative H&E (upper panels) and PAS (lower panels) staining of lung sections from WT, CKO, and CKO+rIL-25 groups, with quantification of inflammation and PAS scores. Scale bar, 100 μm. Statistical analysis: Data are presented as mean ± SD ( n = 5 mice per group). Statistical significance was determined using a two-sided one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001; NS, not significant. Exact P values and complete test statistics for a – h are provided in Supplementary Data . CKO conditional knockout, HDM house dust mite, rIL-25 recombinant IL-25, WT wild-type.

Journal: Nature Communications

Article Title: Airway immune profiles and therapeutic implications of IGF1 in eosinophilic granulomatosis with polyangiitis

doi: 10.1038/s41467-025-68104-6

Figure Lengend Snippet: a – e Anti-IGF1 treatment reduces eosinophilic inflammation and airway remodeling in IL-5 transgenic mice challenged with HDM and IL-33. Mice were divided into Control (PBS-treated), Model (HDM+IL-33 challenged), and Anti-IGF1 (HDM+IL-33+anti-IGF1 antibody) groups. a Total cell counts in bronchoalveolar lavage fluid (BALF) from control, model, and anti-IGF1-treated groups. b Eosinophil percentage in BALF. c Absolute eosinophil counts in BALF. d IL−25 levels in BALF quantified by ELISA. e Representative histological images of lung sections stained with hematoxylin and eosin (H&E, upper panels) and periodic acid-Schiff (PAS, lower panels), with corresponding inflammation and PAS score quantifications. Scale bar, 100 μm. f – h IGF1R deficiency modulates eosinophilic inflammation and airway remodeling via IL−25 in HDM+IL-33 challenged mice. f Total cell counts in BALF from wild-type (WT, Scgb1a1 -IRES-+/+ Igf1r f/f ), conditional knockout ( Scgb1a1 -IRES-Cre/+ Igf1r f/f , CKO), and CKO mice treated with recombinant IL-25 (rIL-25). All groups were challenged with HDM+IL-33. g Flow cytometric analysis of eosinophils (CD45 + Siglec-F + CD11c - ) in BALF. Representative plots and quantification of eosinophil percentages are shown. h Representative H&E (upper panels) and PAS (lower panels) staining of lung sections from WT, CKO, and CKO+rIL-25 groups, with quantification of inflammation and PAS scores. Scale bar, 100 μm. Statistical analysis: Data are presented as mean ± SD ( n = 5 mice per group). Statistical significance was determined using a two-sided one-way ANOVA with Tukey’s post hoc test. * p < 0.05; ** p < 0.01; *** p < 0.001; NS, not significant. Exact P values and complete test statistics for a – h are provided in Supplementary Data . CKO conditional knockout, HDM house dust mite, rIL-25 recombinant IL-25, WT wild-type.

Techniques: Transgenic Assay, Control, Enzyme-linked Immunosorbent Assay, Staining, Knock-Out, Recombinant

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