irf7 shrna plasmid complete kit  (OriGene)

Journal: eBioMedicine

Article Title: Mechanistic analysis of an IRF7-dependent pathway in virus-induced fibrosis in chronic lung allograft dysfunction

doi: 10.1016/j.ebiom.2026.106285

Figure Lengend Snippet: IRF7 and pIRF7 are increased in human CLAD (BOS). (A) Representative Western blot images showing IRF7 and pIRF7 in CLAD (BOS) and Stable LTx whole lung lysates. Densitometric analyses of the above blots (fold change relative to Stable LTx) showing protein expression of (B) IRF7 and (C) pIRF7 in CLAD (BOS) and Stable LTx whole lung tissue (Stable LTx n = 3, CLAD (BOS) n = 4). Error bars represent mean ± SEM. ∗∗p < 0.01, unpaired t-test. (D) Representative immunofluorescence images showing H&E, Trichrome, DAPI (blue), IRF7 (magenta), and merged DAPI/IRF7 channels in Stable LTx and CLAD (BOS) lung tissue sections, demonstrating airway-centric distribution and increased IRF7 expression in CLAD (BOS). (E) Corresponding Integrated Intensity/cell of IRF7 in human CLAD (BOS) and Stable LTx specimens. Each data point represents the mean integrated IRF7 intensity/cell averaged across 3–4 image fields per patient (Stable LTx n = 3, CLAD (BOS) n = 4); group data presented as mean ± SEM; ∗p = 0.017, unpaired t-test.

Article Snippet: IRF7 shRNA plasmid complete kit (Origene, cat. TR315487) was used to suppress IRF7 expression in PCLS and were transfected with either IRF7-specific or control shRNA plasmid in the absence of antibiotics in the culture media.

Techniques: Western Blot, Expressing, Immunofluorescence

Journal: eBioMedicine

Article Title: Mechanistic analysis of an IRF7-dependent pathway in virus-induced fibrosis in chronic lung allograft dysfunction

doi: 10.1016/j.ebiom.2026.106285

Figure Lengend Snippet: Virus exposure induces IRF7 and airway fibrogenesis in the air-liquid-interface PBEC model, and IRF7 silencing attenuates it. (A) Representative Western blots showing protein expression of IRF7, α-SMA, and SMAD2/3 in stably expressing control (Ctr) shRNA and IRF7 shRNA primary bronchial epithelial cell (PBEC) cell line air-liquid-interface (ALI) cultures in the presence and absence of Influenza A virus (IAV). Densitometric analyses of the above blots showing protein expression of (B) IRF7, (C) α-SMA, and (D) SMAD2/3 in Ctr shRNA and IRF7 shRNA PBEC cell line ALI cultures (n = 6 each). Error bars represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, Mann–Whitney test for 2 samples, one way Anova with Tukeys multiple comparison test for >3 groups (E) Sircol assay showing fold change soluble collagen content in the ALI culture supernatants from the above experiments (n = 3 each). Error bars represent mean ± SEM. ∗∗p < 0.01, Mann–Whitney test. (F) Representative immunofluorescence images showing DAPI (blue) and MUC5AC (red) of stably expressing control shRNA and IRF7 shRNA cell line ALI cultures exposed to IAV, demonstrating attenuation of airway mucogenesis with IRF7 silencing.

Article Snippet: IRF7 shRNA plasmid complete kit (Origene, cat. TR315487) was used to suppress IRF7 expression in PCLS and were transfected with either IRF7-specific or control shRNA plasmid in the absence of antibiotics in the culture media.

Techniques: Virus, Western Blot, Expressing, Stable Transfection, Control, shRNA, MANN-WHITNEY, Comparison, Immunofluorescence

Journal: eBioMedicine

Article Title: Mechanistic analysis of an IRF7-dependent pathway in virus-induced fibrosis in chronic lung allograft dysfunction

doi: 10.1016/j.ebiom.2026.106285

Figure Lengend Snippet: Virus exposure induces fibrogenesis and IRF7 blockade attenuates it in the human precision-cut lung slice ex vivo model. (A) Representative immunofluorescence images showing IRF7 (red), α-SMA (green), DAPI (blue), and merged channels in a human precision-cut lung slice (PCLS) model in non-treated (NT) and Influenza A virus (IAV)-exposed conditions. (B) Corresponding fold change fluorescence intensity of IRF7 and α-SMA in the above experiment (n = 5–6 each). Error bars represent mean ± SEM. ∗∗p < 0.01, Mann–Whitney test. (C) Representative immunofluorescence images showing IRF7 (red), DAPI (blue), and merged channels, alongside trichrome staining showing collagen deposition, in IAV-exposed stably expressing control shRNA and IRF7 shRNA PCLS slices. (D) % Area of slices positive for trichrome stain in IAV-exposed stably expressing control shRNA and IRF7 shRNA PCLS slices (n = 5–6 each). Error bars represent mean ± SEM. ∗p < 0.05, Mann–Whitney test.

Article Snippet: IRF7 shRNA plasmid complete kit (Origene, cat. TR315487) was used to suppress IRF7 expression in PCLS and were transfected with either IRF7-specific or control shRNA plasmid in the absence of antibiotics in the culture media.

Techniques: Virus, Ex Vivo, Immunofluorescence, Fluorescence, MANN-WHITNEY, Staining, Stable Transfection, Expressing, Control, shRNA

Journal: eBioMedicine

Article Title: Mechanistic analysis of an IRF7-dependent pathway in virus-induced fibrosis in chronic lung allograft dysfunction

doi: 10.1016/j.ebiom.2026.106285

Figure Lengend Snippet: Virus induces IL-33 via IRF7 and IL-33 blockade attenuates virus-induced fibrogenesis. (A) Representative Western blots showing protein expression of IRF7 and IL-33 in stably expressing control shRNA and IRF7 shRNA primary bronchial epithelial cell (PBEC) cell line air-liquid-interface (ALI) cultures in the presence and absence of Influenza A virus (IAV). (B) Densitometry fold change protein expression of IL-33 in control shRNA and IRF7 shRNA PBEC cell line ALI cultures in the presence and absence of IAV (n = 4 each). Error bars represent mean ± SEM. ∗p < 0.05, 1-way ANOVA with Tukey’s multiple comparison post-test. (C) Representative Western blots showing protein expression of IRF7 and α-SMA in stably expressing control shRNA and IRF7 shRNA PBEC cell line ALI cultures in the presence and absence of IAV and IL-33 blockade. (D) Densitometry fold change of α-SMA protein expression in stably expressing control shRNA and IRF7 shRNA PBEC cell line ALI cultures in the presence and absence of IAV and IL-33 blockade (n = 4 each). Error bars represent mean ± SEM. ∗p < 0.05, ∗∗p < 0.01, ns = not significant, 1-way ANOVA with Tukey’s multiple comparison post-test.

Article Snippet: IRF7 shRNA plasmid complete kit (Origene, cat. TR315487) was used to suppress IRF7 expression in PCLS and were transfected with either IRF7-specific or control shRNA plasmid in the absence of antibiotics in the culture media.

Techniques: Virus, Western Blot, Expressing, Stable Transfection, Control, shRNA, Comparison

Journal: eBioMedicine

Article Title: Mechanistic analysis of an IRF7-dependent pathway in virus-induced fibrosis in chronic lung allograft dysfunction

doi: 10.1016/j.ebiom.2026.106285

Figure Lengend Snippet: MMP-9 blockade attenuates virus-mediated fibrogenesis. (A) Fold change mRNA expression of MMP-9 in stably expressing control shRNA and IRF7 shRNA primary bronchial epithelial cell (PBEC) cell line air-liquid-interface (ALI) cultures in the presence and absence of Influenza A virus (IAV) (n = 3 each). Error bars represent mean ± SEM. ∗∗p < 0.01, Mann–Whitney test. (B) MMP-9 (ng/ml of supernatant) concentrations by ELISA in the lower compartment of control shRNA and IRF7 shRNA PBEC cell line ALI culture medium in the presence and absence of IAV (n = 4 each). Error bars represent mean ± SEM. ∗∗∗∗p < 0.0001, 1-way ANOVA with Tukey’s multiple comparison post-test. (C) MMP-9 (ng/ml of supernatant) concentrations by ELISA in the lower compartment of IAV-exposed PBEC cell line ALI model with and without IL-33 blockade (n = 4 each). Error bars represent mean ± SEM. ∗∗∗∗p < 0.0001, ∗∗p < 0.01, ∗p < 0.05, 1-way ANOVA with Tukey’s multiple comparison post-test. (D) MMP-9 (ng/ml of supernatant) concentrations by ELISA in the lower compartment of IAV-exposed stably expressing IRF7 shRNA PBEC ALI model with and without IL-33 blockade (n = 4 each). Error bars represent mean ± SEM. ∗p < 0.05, ns = not significant, 1-way ANOVA with Tukey’s multiple comparison post-test. (E) Representative Western blots showing protein expression of α-SMA in virus-exposed ALI PBEC model with and without MMP-9 blockade. (F) Densitometry fold change protein expression of α-SMA in IAV-exposed ALI PBEC model with and without MMP-9 blockade (n = 5 each). ∗∗∗∗p < 0.0001, ∗∗p < 0.01, ns = not significant, 1-way ANOVA with Tukey’s multiple comparison post-test.

Article Snippet: IRF7 shRNA plasmid complete kit (Origene, cat. TR315487) was used to suppress IRF7 expression in PCLS and were transfected with either IRF7-specific or control shRNA plasmid in the absence of antibiotics in the culture media.

Techniques: Virus, Expressing, Stable Transfection, Control, shRNA, MANN-WHITNEY, Enzyme-linked Immunosorbent Assay, Comparison, Western Blot

Journal: eBioMedicine

Article Title: Mechanistic analysis of an IRF7-dependent pathway in virus-induced fibrosis in chronic lung allograft dysfunction

doi: 10.1016/j.ebiom.2026.106285

Figure Lengend Snippet: Schematic representation of the pathway involved in virus-induced airway fibrogenesis. (1 and 2) Influenza virus activates IRF7 via the RIG-1/MAVS/TBK1 axis, and activated IRF7 enters the nucleus and induces expression of IL-33. (3 and 4) IL-33 is secreted from the epithelial cells into the interstitial matrix, where it acts upon neighbouring epithelial cells, resident fibroblasts, and other cell types (paracrine), as well as the same cell (autocrine manner). (5) IL-33 induces MMP-9 expression, and MMP-9 is secreted into the interstitial matrix. (6) MMP-9 cleaves latent TGF-β to its active form. (7 and 8) Activated TGF-β induces SMAD2/3 signalling, driving expression of collagens and α-SMA and culminating in fibrogenesis and extracellular matrix remodelling.

Article Snippet: IRF7 shRNA plasmid complete kit (Origene, cat. TR315487) was used to suppress IRF7 expression in PCLS and were transfected with either IRF7-specific or control shRNA plasmid in the absence of antibiotics in the culture media.

Techniques: Virus, Expressing