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Clinical and Diagnostic Laboratory Immunology, May 2002, p. 669-676, Vol. 9, No. 3
1071-412X/02/$04.00+0 DOI: 10.1128/CDLI.9.3.669-676.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Department of First Internal Medicine,1 Department of Infectious Diseaes,2 Department of Pathology, Kyorin University School of Medicine, Tokyo 181-8611, Japan3
Received 10 August 2001/ Returned for modification 6 November 2001/ Accepted 23 January 2002
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 105 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.
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