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Production1
Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912
Viral infections in humans or mice can result in increased
sensitivity to challenges with bacteria, bacterial products, or
cytokine administration. During lymphocytic choriomeningitis virus
infections, mice are more sensitive to the lethal effects of bacterial
endotoxin LPS, and in the experiments reported here, were observed at
up to 10-fold lower doses in infected than in uninfected mice. The
mechanisms responsible for heightened susceptibility under these
conditions were evaluated. Kinetic studies demonstrated that
virus-infected mice had 3- to 50-fold increases over uninfected mice in
peak serum TNF, IL-12, and IFN-
levels after LPS administration. All
three cytokines contributed to lethality during dual challenge, because
neutralization of any one of the factors protected from death.
Production of TNF was not dependent on either NK or T cells. In
contrast, these populations were the predominant sources of IFN-, as
determined by lack of detectable IFN- production in NK and T
cell-deficient mice and by intracellular cytokine expression in the
cell subsets. Concordant with the demonstrations that both cell
populations produced IFN- and that this factor was critical for
lethality, removal of either subset alone was not sufficient to protect
mice from death resulting from dual challenges. Increased resistance
required absence of both cell subsets. Taken together, the data show
that during viral infections, the normally protective immune responses
can profoundly modify reactions to secondary heterologous challenges,
to result in dysregulated cytokine expression and consequent heightened
detrimental effects.
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