Journal: Allergy

Article Title: Acetylcholine From Solitary Chemosensory Cell, Not Neuron, Regulates Basal Cell Fate Driving Eosinophilic Chronic Rhinosinusitis With Nasal Polyps

doi: 10.1111/all.70048

Figure Lengend Snippet: Increased Ach levels in eCRSwNP, predominantly derived from SCC. (A) Histogram showing relative mRNA expression of ChAT and VAchT in bulk RNA‐seq. (B) Histogram showing relative mRNA expression of ChAT and VAchT in control, neCRSwNP, and eCRSwNP tissues through qRT‐PCR analysis ( n = 6 per group). (C) Immunohistochemical staining showing ChAT expression in tissues from control, neCRSwNP, and eCRSwNP groups. (D‐E) Histogram showing ChAT immunoreactivity and positive staining areas in each group of tissues ( n = 8 per group). (F) IF staining of ChAT (red) and the neuronal marker βIII Tublin (green) in control and eCRSwNP tissues. (G) Histogram showing CHAT + βIII Tublin + cell numbers in subepithelium ( n = 8 per group). (H) IF staining of ChAT (red) and the SCC marker GNAT3 (green) in control and eCRSwNP tissues. (I) Histogram showing CHAT + GNAT3 + cell numbers ( n = 8 per group). (J) IF staining showing co‐localization of ChAT (red) with CC marker FOXJ1 (green), GC marker MUC5AC (red), BC marker P63 (green), and SCC marker GNAT3 (green) in ALI cultures. (K) Histogram showing Ach concentrations in the basolateral medium of ALI cultures under the following conditions: Untreated, α‐NETA‐treated, and IL‐4/IL‐5/IL‐13 treatment with or without α‐NETA, as measured by ELISA ( n = 3 per group). Data are presented as mean ± SEM. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: Depending on the experimental condition, the cultures were additionally treated with PBS, 10 μM α‐NETA (HY‐138097, MCE, Monmouth Junction, NJ, USA), 5 ng/mL IL‐4 (HY‐ P70445 , MCE) with or without 10 μM α‐NETA, 5 ng/mL IL‐5 (HY‐ P70612 , MCE) with or without 10 μM α‐NETA, 5 ng/mL IL‐13 (HY‐ P70568 , MCE) with or without 10 μM α‐NETA, or 5 mM acetylcholine chloride (HY‐ P70445 , MCE) with or without 100 nM tiotropium bromide (TB, HY‐17360, MCE).

Techniques: Derivative Assay, Expressing, RNA Sequencing, Control, Quantitative RT-PCR, Immunohistochemical staining, Staining, Marker, Enzyme-linked Immunosorbent Assay

Journal: Nature communications

Article Title: Epithelial SIRT6 governs IL-17A pathogenicity and drives allergic airway inflammation and remodeling.

doi: 10.1038/s41467-023-44179-x

Figure Lengend Snippet: Fig. 7 | The SIRT6 inhibitor OSS_128167 (OSS) preventes airway remodeling in asthmatic mice. a Chemical Structure of OSS_128167 (OSS) is shown. b Schematic overview of experimental design for (b–j) in an ASA model. c Representative photomicrographs of lung inflammation expression are shown (Control n = 4; HDM + LPS n = 5, HDM + LPS + OSS n = 6). Scale bars, 100 μm. d, e The expression of RORγt, SIRT6, and IL-17A in the lung homogenate from mice treated with HDM/LPS or mice treated with HDM/LPS and SIRT6 inhibitor OSS_128167 (OSS) was analyzed by using Western blot. Quantification was analyzed by Image J software. f, g ELISA and qRT-PCR analysis of IL-17A in lung homogenate of mice. h–j The expression of inflammatory cytokines in the lung homogenate of mice was analyzed by using qRT-PCR or ELISA analysis. k Schematic overview of experimental design for (L-O)

Article Snippet: Human IL-17A, mouse IL-17A, CXCL1, CXCL2, IL-5, and IL-13 were measured using ELISA kit (Elabscience, China).

Techniques: Expressing, Control, Western Blot, Software, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR