Identification of a mechanism for lung inflammation caused by Mycoplasma pneumoniae using a novel mouse model

Results in immunology Pub Date : 2011-05-01 Epub Date: 2011-11-11 DOI:10.1016/j.rinim.2011.11.001
Takeshi Saraya , Koh Nakata , Kazuhide Nakagaki , Natsuki Motoi , Kuniko Iihara , Yasunori Fujioka , Teruaki Oka , Daisuke Kurai , Hiroo Wada , Haruyuki Ishii , Haruhiko Taguchi , Shigeru Kamiya , Hajime Goto
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引用次数: 20

Abstract

Human Mycoplasma pneumoniae (MP) pneumonia is characterized by alveolar infiltration with neutrophils and lymphocytes and lymphocyte/plasma cell infiltrates in the peri-bronchovascular area (PBVA). No mouse model has been able to mimic the pathological features seen in human MP pneumonia, such as plasma cell-rich lymphocytic infiltration in PBVA. To figure out the mechanism for inflammation by MP infection using a novel mouse model that mimics human MP pneumonia, mice were pre-immunized intraperitoneally with Th2 stimulating adjuvant, alum, alone or MP extracts with an alum, followed by intratracheal challenge with MP extracts. The toll-like receptor-2, which is the major receptor for mycoplasma cell wall lipoproteins, was strongly up-regulated in alveolar macrophages in a latter group after the pre-immunization but prior to the intratracheal challenge. Those findings demonstrated that acceleration of innate immunity by antecedent antigenic stimulation can be an important positive-feedback mechanism in lung inflammation during MP pneumonia.

利用新型小鼠模型鉴定肺炎支原体引起肺部炎症的机制
人肺炎支原体肺炎的特征是肺泡浸润中性粒细胞和淋巴细胞,支气管血管周围区(PBVA)有淋巴细胞/浆细胞浸润。没有小鼠模型能够模拟人类MP肺炎的病理特征,如PBVA中富含浆细胞的淋巴细胞浸润。为了研究MP感染引起炎症的机制,我们建立了一种模拟人MP肺炎的新型小鼠模型,通过腹腔注射Th2刺激佐剂、明矾、单独或明矾提取物预免疫小鼠,然后气管内注射MP提取物。toll样受体-2是支原体细胞壁脂蛋白的主要受体,在后一组的肺泡巨噬细胞中,在预免疫后但在气管内刺激之前被强烈上调。这些发现表明,在MP肺炎期间,预先抗原刺激的先天免疫加速可能是一个重要的正反馈机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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