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-T Cells Are Critical for Survival and Early Proinflammatory Cytokine Gene Expression During Murine Klebsiella Pneumonia1
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, MI 48109
Although cells of the innate inflammatory response, such as
macrophages and neutrophils, have been extensively studied in the arena
of Gram-negative bacterial pneumonia, a role for T cells remains
unknown. To study the role of specific T cell populations in bacterial
pneumonia, mice deleted of their TCR ß- and/or 
-chain were
intratracheally inoculated with Klebsiella pneumoniae.
T cell knockout mice displayed increased mortality at both early
and late time points. In contrast, mice specifically lacking only
ß-T cells were no more susceptible than wild-type mice. Pulmonary
bacterial clearance in -T cell knockout mice was unimpaired.
Interestingly, these mice displayed increased peripheral blood
dissemination. Rapid up-regulation of IFN- and TNF- gene
expression, critical during bacterial infections, was markedly impaired
in lung and liver tissue from -T cell-deficient mice 24 h
postinfection. The increased peripheral blood bacterial dissemination
correlated with impaired hepatic bacterial clearance following
pulmonary infection and increased hepatic injury as measured by plasma
aspartate aminotransferase activity. Combined, these data suggest that
mice lacking -T cells have an impaired ability to resolve
disseminated bacterial infections subsequent to the initial pulmonary
infection. These data indicate that -T cells comprise a critical
component of the acute inflammatory response toward extracellular
Gram-negative bacterial infections and are vital for the early
production of the proinflammatory cytokines IFN- and
TNF-.
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