脂多糖通过IL - 13和肺巨噬细胞激活共同诱导变应性气道疾病小鼠模型中的类固醇抵抗性恶化

S. Hadjigol, Keilah G. Netto, S. Maltby, H. Tay, T. H. Nguyen, Nicole G. Hansbro, F. Eyers, P. Hansbro, Ming Yang, P. Foster
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引用次数: 25

摘要

哮喘急性加重是疾病的主要负担,通常由呼吸道感染引起。病毒感染被认为是疾病恶化的重要诱因;然而,对微生物生物产物如内毒素(脂多糖)如何引发发作知之甚少。事实上,脂多糖水平的升高与哮喘的发病、严重程度和类固醇耐药性有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lipopolysaccharide induces steroid‐resistant exacerbations in a mouse model of allergic airway disease collectively through IL‐13 and pulmonary macrophage activation
Acute exacerbations of asthma represent a major burden of disease and are often caused by respiratory infections. Viral infections are recognized as significant triggers of exacerbations; however, less is understood about the how microbial bioproducts such as the endotoxin (lipopolysaccharide (LPS)) trigger episodes. Indeed, increased levels of LPS have been linked to asthma onset, severity and steroid resistance.
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