Identification of a mechanism for lung inflammation caused by Mycoplasma pneumoniae using a novel mouse model.
Identification of a mechanism for lung inflammation caused by Mycoplasma pneumoniae using a novel mouse model.
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DOI：
10.1016/j.rinim.2011.11.001
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发表时间：
2011-01-01
期刊：
影响因子：
--
通讯作者：
Goto, Hajime
中科院分区：
文献类型：
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作者：
Saraya, Takeshi;Nakata, Koh;Goto, Hajime
人肺炎支原体（MP）肺炎的特征是支气管血管周围区域（PBVA）的中性粒细胞和淋巴细胞肺泡浸润以及淋巴细胞/浆细胞浸润。没有小鼠模型能够模拟在人MP肺炎中观察到的病理特征，例如PBVA中富含浆细胞的淋巴细胞浸润。为了使用模拟人MP肺炎的新型小鼠模型来弄清楚MP感染引起炎症的机制，将小鼠用Th 2刺激佐剂、单独的明矾或MP提取物与明矾腹膜内预免疫，然后用MP提取物进行腹膜内攻击。Toll样受体-2，这是支原体细胞壁脂蛋白的主要受体，强烈上调肺泡巨噬细胞在后一组的预免疫后，但之前的intrichelheal的挑战。这些发现表明，先天免疫的加速由先行抗原刺激可能是一个重要的正反馈机制，在肺炎支原体肺炎的肺部炎症。
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.