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The Journal of Immunology, 2000, 164: 4812-4818.
Copyright © 2000 by The American Association of Immunologists

Regulation and Role of IFN-{gamma} in the Innate Resistance to Infection with Chlamydia pneumoniae1

Martín E. Rottenberg2, Antonio Gigliotti Rothfuchs, Dulceaydee Gigliotti, Monica Ceausu, Clas Une, Victor Levitsky and Hans Wigzell

Microbiology and Tumorbiology Center, Karolinska Institutet, Stockholm, Sweden

By using mice genomically lacking IFN-{gamma}R, IL-12, perforin, and recombination-activating gene-1 (RAG-1), we analyzed the regulation and importance of IFN-{gamma} 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-{gamma} mRNA. In turn, IFN-{gamma} 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-{gamma}R-/- mice we showed that IFN-{gamma} 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-{gamma} 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-{gamma} during the bacterial infection.




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