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*
Laboratory for Infection and Immunity,
Department of Medical Microbiology, and
Department of Pathology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada
We previously reported that higher IL-10 production is correlated
with lower IFN-
production, weaker delayed hypersensitivity (DTH),
and slower organism clearance following chlamydial infection in mice.
To assess more directly the role of IL-10, we examined protective
immunity and pathological reaction in C57BL/6 IL-10 gene knockout (KO)
and wild-type mice. The results showed that in the absence of
endogenous IL-10, mice had significantly accelerated chlamydial
clearance and developed significantly stronger DTH responses, which
could be inhibited by local delivery of rIL-10. Consistent with the
enhancement of DTH responses, IL-10 KO mice showed stronger and more
persistent CD4 T cell-dependent IFN- production and significant
elevation of IL-12 and TNF-
production. Additionally, wild-type, but
not IL-10 KO, mice showed granuloma formation that was correlated with
higher levels of Th2 cytokine (IL-5) production at the later stages of
infection. Moreover, chlamydial infection, unlike parasitic protozoan
infection, did not induce significant acute toxicity in IL-10 KO mice,
which may be due to the low (undetectable) levels of systemic release
of proinflammatory cytokines. These results suggest that IL-10 inhibits
the priming and expansion of Th1-like T cell responses and that IL-10
plays a role in the fibrotic reaction seen with chlamydial
infection.
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