IL-17A-Induced Redox Imbalance and Inflammatory Responses in Mice Lung via Act1-TRAF6-IKBα Signaling Pathway: Implications for Lung Disease Pathogenesis

被引:1
作者
Panda, Ekta Swarnamayee [1 ]
Gautam, Avtar Singh [1 ]
Pandey, Shivam Kumar [1 ]
Singh, Rakesh Kumar [1 ]
机构
[1] Natl Inst Pharmaceut Educ & Res NIPER Raebareli, Dept Pharmacol & Toxicol, Transit Campus,Bijnour Sisendi Rd, Lucknow 226002, Uttar Pradesh, India
关键词
Lung inflammation; Interleukin-17A; IL-17; receptor; Animal model; IL-17-Act1; pathway; OXIDATIVE STRESS; SEVERE ASTHMA; IL-17A; INTERLEUKIN-17; CYTOKINES; CELLS; EXACERBATION; CONTRIBUTES; GLUTATHIONE; ACTIVATION;
D O I
10.1007/s10753-024-02199-9
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
IL-17A is a potent proinflammatory cytokine that plays a crucial role in the pathogenesis of various lung diseases. This study focused on the evaluation of the role of IL-17 receptor signaling through one-week intranasal exposure of IL-17A in lung tissues of BALB/c mice. IL-17A triggered inflammatory responses in the mice lungs and led to changes in the morphological alveolar arrangements. Exposure of IL-17A induced redox imbalance by triggering an increase in the level of the pro-oxidants (reactive oxygen species, nitrite and malondialdehyde) and reduction of the levels of antioxidant proteins (glutathione, superoxide dismutase and catalase) in the lung tissue. IL-17A also caused a significant elevation in the levels of proinflammatory cytokines lines including TNF-alpha, IL-1 beta and IL-6, in lung tissue as well as in plasma. More interestingly, these changes were accompanied by the alterations in IL-17 receptor downstream signaling through activation of IL-17R-Act1-TRAF6-IKB alpha-mediated pathway. IL-17A exposure also caused lung tissue injury, recruitment and polarization of immune cells from anti-inflammatory to pro-inflammatory. This study clearly demonstrated the role of IL-17A-induced signaling in worsening lung inflammatory diseases, and hence points towards its emergence as an important therapeutic target to control lung inflammation.
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页数:14
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