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*Pneumocystis Infections
The Journal of Immunology, 2003, 171: 4700-4707.
Copyright © 2003 by The American Association of Immunologists

TNF-{alpha}-Dependent ICAM-1- and VCAM-1-Mediated Inflammatory Responses Are Delayed in Neonatal Mice Infected with Pneumocystis carinii 1

Mahboob H. Qureshi*,{ddagger}, Joan Cook-Mills§, Dennis E. Doherty{dagger},{ddagger} and Beth A. Garvy2,*,{dagger},{ddagger}

Departments of * Microbiology, Immunology, and Molecular Genetics and {dagger} Internal Medicine, University of Kentucky, and {ddagger} Veterans Administration Medical Center, Lexington, KY 40536; and § Department of Pathology, University of Cincinnati, Cincinnati, OH 45267

Neonatal mice have a delayed CD4-mediated inflammatory response to Pneumocystis carinii (PC) infection in the lungs that corresponds to a delayed TNF-{alpha} response and a delayed clearance of the organisms compared with adult mice. Since TNF-{alpha} is known to drive the up-regulation of adhesion molecules, we examined the expression and function of adhesion molecules in the lungs of neonatal mice. The expression of both ICAM-1 and VCAM-1 was significantly lower in the lungs of PC-infected neonatal mice compared with adults. Additionally, migration of neonatal T cells across endothelial cells expressing VCAM-1 and monocyte chemotactic protein-1 was aberrant compared with that in adult T cells, although {alpha}4{beta}1 integrin-mediated adhesion of neonatal lymphocytes was comparable to that of adult lymphocytes. Treatment of neonatal mice with exogenous TNF-{alpha} resulted in increased expression of ICAM-1 and VCAM-1 as well as increased expression of chemokines, resulting in infiltration of CD4+ cells into the lungs. Treatment with exogenous TNF-{alpha} resulted in a trend (although not statistically significant) toward a reduction of PC organisms from the lungs. These data indicate that neonatal lung endothelial cells do not up-regulate ICAM-1 and VCAM-1 in response to PC infection, probably due to depressed TNF-{alpha} production. Additionally, neonatal T cells are defective in the ability to migrate across endothelial cells.




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