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首页> 外文期刊>American Journal of Physiology >The relationship between complement C3 expression and the MUC5B genotype in pulmonary fibrosis
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The relationship between complement C3 expression and the MUC5B genotype in pulmonary fibrosis

机译：补体C3表达与肺纤维化中的MUC5B基因型的关系

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摘要

The common gain-of-function MUC5B promoter variant (rs35705950) is the strongest risk factor for the development of idiopathic pulmonary fibrosis (IPF). While the role of complement in IPF is controversial, both MUC5B and the complement system play a role in lung host defense. The aim of this study was to evaluate the relationship between complement component 3 (C3) and MUC5B in patients with IPF and in bleomycin-induced lung injury in mice. To do this, we evaluated C3 gene expression in whole lung tissue from 300 subjects with IPF and 175 healthy controls. Expression of C3 was higher in IPF than healthy controls (1.40-fold increase [95% confidence interval (CI) 1.31-1.50]; P < 0.0001} and even greater among IPF subjects with the highest-risk IPF MUC5B promoter genotype [TT vs. GG = 1.59-fold (95% CI 1.15-2.20); P < 0.05; TT vs. GT = 1.66-fold (95% CI 1.20-2.30); P < 0.05]. Among subjects with IPF, C3 expression was significantly higher in the lung tissue without microscopic honeycombing than in the lung tissue with microscopic honeycombing [1.40-fold increase (95% CI 1.23- 1.59); P < 0.01]. In mice, while bleomycin exposure increased Muc5b protein expression, C3-deficient mice were protected from bleomycin-induced lung injury. In aggregate, our findings indicate that the MUC5B promoter variant is associated with higher C3 expression and suggest that the complement system may contribute to the pathogenesis of IPF.
机译：常见的功能增益MUC5B启动子变体（RS35705950）是发作性肺纤维化（IPF）的发展的最强风险因素。虽然IPF补充的作用是有争议的，但MUC5B和补充系统都在肺主机防御中发挥作用。本研究的目的是评估IPF患者的补体组分3（C3）和MUC5B之间的关系，并在小鼠中含有博来霉素诱导的肺损伤。为此，我们评估了来自IPF和175个健康对照的300个受试者的整肺组织中的C3基因表达。 IPF的表达高于健康对照（1.40倍的增加[95％置信区间（CI）1.31-1.50]; P <0.0001}，在具有最高风险IPF MUC5B启动子基因型的IPF受试者中，甚至更大甚至更大。GG = 1.59倍（95％CI 1.15-2.20）; P <0.05; TT与GT = 1.66倍（95％CI 1.20-2.30）; P <0.05]。在具有IPF的受试者中，C3表达显着在没有微观蜂窝状的情况下肺组织比在肺组织中高于微观蜂窝状的肺组织[1.40倍，增加（95％CI 1.23- 1.59）;在小鼠中，玻璃霉素暴露增加了MUC5B蛋白表达，C3缺陷小鼠被保护免受Bleomycin诱导的肺损伤。在骨料中，我们的研究结果表明，MUC5B启动子变体与较高的C 3表达有关，并表明补体系统可能有助于IPF的发病机制。

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