IL-17A deficiency alleviates PM-induced allergic asthma by suppressing Th17 cell secretion cytokines and mucus overproduction

نویسندگان

چکیده

Abstract Particulate matter (PM) aggravates airway and lung inflammatory response in allergic asthma by directly inducing Th17 cells to secrete cell-associated factors chemokines. IL-17A is a key cell secretion pro-inflammatory cytokine. In this study, we investigated the role of PM-induced mice. 7–8 weeks old wild type (WT) mice, similarly knockout (KO) were divided into four experimental groups (healthy control, PM only, OVA OVA+PM treatment groups) treated accordingly. Inflammatory eosinophil infiltration increased WT mice compared healthy but decreased KO Among toll-like receptors (TLRs) that play an important innate immune response, TLR2/4/7 expression was significantly reduced Furthermore, observed decrease mRNA IL-13, IL-17A, IL-22, TGF-β among cytokines Th2 facilitated overt histopathological symptoms such as mucus overproduction goblet hyperplasia while showed mitigated responses These results prove plays pathogenesis asthma. This research funded Ministry Education. Education

برای دانلود باید عضویت طلایی داشته باشید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

IL-37 Alleviates Rheumatoid Arthritis by Suppressing IL-17 and IL-17-Triggering Cytokine Production and Limiting Th17 Cell Proliferation.

IL-37, a new member of the IL-1 cytokine family, is a natural inhibitor of innate immunity associated with autoimmune diseases. This study was undertaken to evaluate whether IL-37 has antiarthritic effects in patients with rheumatoid arthritis (RA) and in mice with collagen-induced arthritis (CIA). In this study, we analyzed the expression of IL-37 in PBMCs, serum, and lymphocytes from RA patie...

متن کامل

5-BDBD ameliorates an OVA-induced allergic asthma by the reduction of Th2 cytokines production

Objective(s): P2X4R is expressed in immunocyte and lung tissues. It has been a focus in inflammatory responses recently. This study investigated whether blockage of P2X4R attenuates allergic inflammation by modulating T cell response in ovalbumin-sensitized mice. Materials and Methods: Ovalbumin was used to sensitize and challenge for a mouse model. Intranasal application of 5-BDBD, P2X4R antag...

متن کامل

IL-13 regulates Th17 secretion of IL-17A in an IL-10-dependent manner.

IL-13 is a central mediator of airway hyperresponsiveness and mucus expression, both hallmarks of asthma. IL-13 is found in the sputum of patients with asthma; therefore, IL-13 is an attractive drug target for treating asthma. We have shown previously that IL-13 inhibits Th17 cell production of IL-17A and IL-21 in vitro. Th17 cells are associated with autoimmune diseases, host immune responses,...

متن کامل

Bifidobacterium longum Alleviates Dextran Sulfate Sodium-Induced Colitis by Suppressing IL-17A Response: Involvement of Intestinal Epithelial Costimulatory Molecules

Although some bacterial strains show potential to prevent colitis, their mechanisms are not fully understood. Here, we investigated the anti-colitic mechanisms of Bifidobacterium longum subsp. infantis JCM 1222(T), focusing on the relationship between interleukin (IL)-17A secreting CD4(+) T cells and intestinal epithelial costimulatory molecules in mice. Oral administration of JCM 1222(T) to mi...

متن کامل

IL-27 alleviates the bleomycin-induced pulmonary fibrosis by regulating the Th17 cell differentiation

BACKGROUND Interleukin-27 (IL-27) is a multifunctional cytokine with both pro-inflammatory and immunoregulatory functions. At present, the role of IL-27 in pulmonary fibrosis remains unknown. METHODS In this study, we observed the expression of IL-27/IL-27R in a mouse model of bleomycin (BLM)-induced pulmonary fibrosis. We verified the role of IL-27 using hematoxylin and eosin as well as Mass...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

ژورنال

عنوان ژورنال: Journal of Immunology

سال: 2023

ISSN: ['1550-6606', '0022-1767']

DOI: https://doi.org/10.4049/jimmunol.210.supp.67.20