Mycoplasma pneumoniae infection increases airway collagen deposition in a murine model of allergic airway inflammation
Mycoplasma pneumoniae infection increases airway collagen deposition in a murine model of allergic airway inflammation
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DOI：
10.1152/ajplung.00167.2004
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发表时间：
2005-07-01
影响因子：
4.9
通讯作者：
Martin, RJ
中科院分区：
文献类型：
--
作者：
Chu, HW;Rino, JG;Martin, RJ
放大图片作者：John G.里诺，瑞秋B。Wexler，Krista坎贝尔，罗纳德J. Harbeck和Richard J. Martin。肺炎支原体感染增加过敏性气道炎症小鼠模型气道胶原沉积。美国生理学杂志肺细胞分子生理学289：L125-L133，2005年。首次发表于2005年3月18日; doi：10.1152/ajplung.00167.2004。肺炎支原体（Mp）与慢性哮喘有关。气道重塑（e.例如，在一个实施例中，气道胶原沉积或纤维化）是慢性哮喘的病理特征之一。然而，呼吸道Mp感染对哮喘气道纤维化的影响尚不清楚。在本研究中，我们假设呼吸道MP感染可能会增加过敏性气道炎症小鼠模型中的气道胶原沉积，部分是通过上调转化生长因子（TGF）-β 1。给予小鼠MP或盐水（对照）的双重（间隔2周）接种，有或没有以前的过敏原（卵清蛋白）的挑战。在最后一次Mp或生理盐水后第14天和第42天，收集肺组织和支气管肺泡灌洗液（BAL）用于蛋白质和mRNA水平的胶原蛋白和TGF-β 1分析。在未接触过过敏原的小鼠中，MP不改变气道壁胶原。在过敏原激发的小鼠中，MP感染在第14天没有改变气道壁胶原沉积，但在第42天增加了气道胶原;这种增加伴随着气道壁中TGF-β 1蛋白的增加和肺组织向BAL液中TGF-β 1蛋白释放的减少。我们的研究结果表明，MP感染可以调节过敏性气道炎症与TGF-β 1参与胶原沉积过程的小鼠模型中的气道胶原沉积。
Chu, Hong Wei, John G. Rino, Rachel B. Wexler, Krista Campbell, Ronald J. Harbeck, and Richard J. Martin. Mycoplasma pneumoniae infection increases airway collagen deposition in a murine model of allergic airway inflammation. Am J Physiol Lung Cell Mol Physiol 289: L125-L133, 2005. First published March 18, 2005; doi:10.1152/ajplung.00167.2004.-Mycoplasma pneumoniae (Mp) has been linked to chronic asthma. Airway remodeling (e. g., airway collagen deposition or fibrosis) is one of the pathological features of chronic asthma. However, the effects of respiratory Mp infection on airway fibrosis in asthma remain unclear. In the present study, we hypothesized that respiratory Mp infection may increase the airway collagen deposition in a murine model of allergic airway inflammation in part through upregulation of transforming growth factor (TGF)-beta 1. Double (2 wk apart) inoculations of Mp or saline (control) were given to mice with or without previous allergen (ovalbumin) challenges. On days 14 and 42 after the last Mp or saline, lung tissue and bronchoalveolar lavage (BAL) fluid were collected for analyses of collagen and TGF-beta 1 at protein and mRNA levels. In allergen-naive mice, Mp did not alter airway wall collagen. In allergen-challenged mice, Mp infections did not change airway wall collagen deposition on day 14 but increased the airway collagen on day 42; this increase was accompanied by increased TGF-beta 1 protein in the airway wall and reduced TGF-beta 1 protein release from the lung tissue into BAL fluid. Our results suggest that Mp infections could modulate airway collagen deposition in a murine model of allergic airway inflammation with TGF-beta 1 involved in the collagen deposition process.