Saraya Takeshi, Nakata Koh, Nakagaki Kazuhide, Motoi Natsuki, Iihara Kuniko, Fujioka Yasunori, Oka Teruaki, Kurai Daisuke, Wada Hiroo, Ishii Haruyuki, Taguchi Haruhiko, Kamiya Shigeru, Goto Hajime
Department of Respiratory Medicine, Kyorin University School of Medicine, 6-20-2, Shinkawa, Mitaka City, Tokyo, Japan.
Niigata University Medical & Dental Hospital, Bioscience Medical Research Center, 1-754, Asashimachi-dori, Chuo-ku, Niigata 951-8520, Japan.
Results Immunol. 2011 Nov 11;1(1):76-87. doi: 10.1016/j.rinim.2011.11.001. eCollection 2011.
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.
人肺炎支原体（MP）肺炎的特征是肺泡中有中性粒细胞和淋巴细胞浸润，支气管血管周围区域（PBVA）有淋巴细胞/浆细胞浸润。尚无小鼠模型能够模拟人MP肺炎中所见的病理特征，如PBVA中富含浆细胞的淋巴细胞浸润。为了利用一种模拟人MP肺炎的新型小鼠模型来弄清楚MP感染引发炎症的机制，将小鼠腹腔内预先单独用Th2刺激佐剂明矾免疫，或用明矾与MP提取物一起免疫，随后气管内给予MP提取物攻击。在预先免疫后但气管内攻击前，后一组小鼠肺泡巨噬细胞中作为支原体细胞壁脂蛋白主要受体的Toll样受体2被强烈上调。这些发现表明，先前的抗原刺激加速固有免疫可能是MP肺炎期间肺部炎症的一种重要正反馈机制。
