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Departments of
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Pediatrics,
Microbiology and Immunology,
Human Biological Chemistry and Genetics,
§
Pathology,
¶
Preventive Medicine and Community Health, and
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Sealy Center for Molecular Sciences, University of Texas Medical Branch, Galveston, TX 77555; and
#
Department of Surgery, University of Wisconsin, Madison, WI 53706
IL-10 plays an important role in preventing excessive inflammation
to the normal flora in the intestinal lumen. The purpose of this study
was to compare the effect of normal flora on inflammation in mice in
which the IL-10 gene was disrupted. IL-10 knock-out mice housed in
germfree conditions remained healthy while those housed in conventional
conditions developed colitis after weaning, suggesting that IL-10
inhibits the adverse responses to luminal Ag. Crypt abscesses were
present in virtually all of the diseased animals as evidenced by
flattening of the epithelial cells and a large number of neutrophils in
the lumen of the crypt. Since KC is a chemokine that is capable of
recruiting neutrophils in mice, mRNA and protein for KC was measured.
Increased levels of both KC mRNA and protein were detected in the colon
of diseased mice. To determine whether the epithelial cells were
capable of synthesizing KC and contributing to neutrophil accumulation
in the crypts, a murine intestinal epithelial cell line (Mode-K) was
shown to express mRNA and protein for KC. Two cytokines induced in
association with colitis in these mice, TNF-
and IFN-
, increased
the expression of KC mRNA and protein in murine epithelial cells.
However, IL-10 was incapable of decreasing the induction of KC, even
though the cells expressed the IL-10 receptor. These results suggest
that the neutrophil chemokine KC is produced by gastrointestinal
epithelial cells in response to inflammatory mediators that are
expressed following exposure to normal flora in animals lacking
IL-10.
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