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,
Departments of
* Internal Medicine and
Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, KY 40536;
Veterans Affairs Medical Center, Lexington, KY 40507; and
Department of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717
Host responses to Pneumocystis carinii infection
mediate impairment of pulmonary function and contribute to the
pathogenesis of pneumonia. IL-10 is known to inhibit inflammation and
reduce the severity of pathology caused by a number of infectious
organisms. In the present studies, IL-10-deficient (IL-10 knockout
(KO)) mice were infected with P. carinii to determine
whether the severity of pathogenesis and the efficiency of clearance of
the organisms could be altered in the absence of IL-10. The clearance
kinetics of P. carinii from IL-10 KO mice was
significantly enhanced compared with that of wild-type (WT) mice. This
corresponded to a more intense CD4+ and CD8+ T
cell response as well as an earlier neutrophil response in the lungs of
IL-10 KO mice. Furthermore, IL-12, IL-18, and IFN-
were found in the
bronchoalveolar lavage fluids at earlier time points in IL-10 KO mice
suggesting that alveolar macrophages were activated earlier than in WT
mice. However, when CD4+ cells were depleted from P.
carinii-infected IL-10 KO mice, the ability to enhance
clearance was lost. Furthermore, CD4-depleted IL-10 KO mice had
significantly more lung injury than CD4-depleted WT mice even though
the intensity of the inflammatory responses was similar. This was
characterized by increased vascular leakage, decreased oxygenation, and
decreased arterial pH. These data indicate that IL-10 down-regulates
the immune response to P. carinii in WT mice; however,
in the absence of CD4+ T cells, IL-10 plays a critical role
in controlling lung damage independent of modulating the inflammatory
response.
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