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使用无菌小鼠建立肺炎支原体感染的动物模型。

Animal model of Mycoplasma pneumoniae infection using germfree mice.

作者信息

Hayakawa Masayuki, Taguchi Haruhiko, Kamiya Shigeru, Fujioka Yasunori, Watanabe Hidehiro, Kawai Shin, Kobayashi Hiroyuki

机构信息

Department of First Internal Medicine, Kyorin University School of Medicine, Tokyo 181-8611, Japan.

出版信息

Clin Diagn Lab Immunol. 2002 May;9(3):669-76. doi: 10.1128/cdli.9.3.669-676.2002.

Abstract

We have attempted to establish a gnotobiotic mouse model monoassociated with Mycoplasma pneumoniae following single or repeated infection to examine the mechanism of pathogenesis following M. pneumoniae infection. M. pneumoniae inoculated into germfree mice colonized equally well at 10(5) CFU/lung in both single infection and repeated infection. In histopathological observation, repeatedly infected mice showed pneumonia with mild infiltration of mononuclear cells and macrophages. Antibody titers against M. pneumoniae rose in the repeatedly infected mice but not in the singly infected mice. The percentage of CD4-positive, CD8-positive, and CD25-positive lymphocytes infiltrated in the lung was increased in the repeatedly infected mice. In contrast, the lymphocyte subset in the spleen was not significantly different among mock-, singly, and repeatedly infected mice. In the study of cytokine productivity of spleen cells, production of interleukin (IL)-4 and IL-10 was significantly increased and that of gamma interferon was remarkably increased in the mice following repeated infection. These results indicate that a gnotobiotic mouse model monoassociated with M. pneumoniae was established and that immune mechanisms might be involved in the pathogenesis in pneumonia following M. pneumoniae infection.

摘要

我们试图建立一种单克隆感染肺炎支原体的悉生小鼠模型,通过单次或重复感染来研究肺炎支原体感染后的发病机制。接种到无菌小鼠体内的肺炎支原体,在单次感染和重复感染中,以10(5) CFU/肺的剂量定殖效果相同。组织病理学观察显示,重复感染的小鼠出现肺炎,伴有单核细胞和巨噬细胞的轻度浸润。重复感染的小鼠体内抗肺炎支原体抗体滴度升高,而单次感染的小鼠则未升高。重复感染的小鼠肺内浸润的CD4阳性、CD8阳性和CD25阳性淋巴细胞百分比增加。相比之下,假感染、单次感染和重复感染的小鼠脾脏中的淋巴细胞亚群没有显著差异。在对脾细胞细胞因子产生能力的研究中,重复感染后的小鼠白细胞介素(IL)-4和IL-10的产生显著增加,γ干扰素的产生显著增加。这些结果表明,已建立了一种单克隆感染肺炎支原体的悉生小鼠模型,并且免疫机制可能参与了肺炎支原体感染后肺炎的发病过程。

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