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1
Institute of Medical Microbiology and Immunology, University of Copenhagen, Copenhagen, Denmark
LPS is the major active agent in the pathogenesis of Gram-negative
septic shock. In this report we have studied the influence of
concurrent viral infection on the outcome of LPS-induced shock. We find
that infection with vesicular stomatitis virus sensitizes mice to LPS
at an early time point following infection. Treatment of mice with the
chemical IFN inducer, polyinosinic:polycytidylic acid, has a similar
effect. This hypersensitivity to LPS correlated with hyperproduction of
TNF-
in vivo. The cellular and molecular mechanisms underlying this
phenomenon were investigated using Ab-depleted and gene-targeted mice.
Our results revealed that while NK cell depletion and elimination of
IFN-
partially protected against the sensitizing effects of
vesicular stomatitis virus and polyinosinic:polycytidylic acid, the
most striking effect was observed in IFN-
R-deficient mice. Thus
hyperproduction of TNF- was completely abrogated in
IFN-R-deficient mice, indicating that the principal mechanism
underlying rapid virus-induced sensitization to LPS is an
IFN--mediated priming of mice for an augmented production of
TNF- in response to LPS. This conclusion was further supported by
the finding that pretreatment of mice with rIFN- mimicked the
effect of viral infection. In conclusion, our results reveal a
previously unrecognized proinflammatory effect of IFN- and point
to a new pathway through which viral infection may influence the
outcome of concurrent bacterial infection.
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