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in the Innate Resistance to Infection with Chlamydia pneumoniae1
Microbiology and Tumorbiology Center, Karolinska Institutet, Stockholm, Sweden
By using mice genomically lacking IFN-
R, IL-12, perforin, and
recombination-activating gene-1 (RAG-1), we analyzed the regulation and
importance of IFN- in the control of infection with
Chlamydia pneumoniae. IL-12 participates
in resistance of mice to C. pneumoniae, probably by
regulating the protective levels of IFN- mRNA. In turn, IFN- is
necessary for the increased IL-12p40 mRNA accumulation that occurs in
lungs during infection with C. pneumoniae, suggesting a
positive feedback regulation between these two cytokines. In
experiments including RAG-1-/-/IFN-R-/-
mice we showed that IFN- produced by innate cells controls the
bacterial load and is necessary for the increased accumulation of
transcripts for enzymes controlling high output NO release (inducible
NO synthase), superoxide production (gp-91 NADPH oxidase), and
catalyzis of tryptophan (indoleamine 2,3-dioxygenase (IDO)), mechanisms
probably related to bacterial killing. Adaptive immune reponses
diminish the levels of IFN- and IL-12 mRNA and thereby the levels of
inducible NO synthase, IDO, and gp91 NADPH oxidase trancripts. By using
RAG-1-/-/perforin-/- mice, we excluded the
overt participation of NK cell cytotoxicity in the control of C.
pneumoniae. However, NK cells and probably other innate immune
cells release IFN- during the bacterial
infection.
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