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*
Department of Internal Medicine,
Division of Gastroenterology, and
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110
The mechanisms allowing the gastrointestinal immune system to avoid
an inappropriate inflammatory response to nonpathogenic luminal Ags are
poorly understood. We have previously described a role for
cyclooxygenase (COX)-2-dependent arachidonic acid metabolites produced
by the murine small intestine lamina propria in controlling the immune
response to a dietary Ag. To better understand the role of
COX-2-dependent arachidonic acid metabolites produced by the lamina
propria, we examined the pattern of expression and the cellular source
of COX-2 and COX-2-dependent PGE2. We now demonstrate that
non-bone marrow-derived lamina propria stromal cells have basal COX-2
expression and that COX-2-dependent PGE2 production by
these cells is spontaneous and continuous. The other mucosal and
nonmucosal lymphoid compartments examined do not share this phenotype.
In contrast to the majority of descriptions of COX-2 expression, COX-2
expression by lamina propria stromal cells is not dependent upon
exogenous stimuli, including adhesion, LPS signaling via Toll-like
receptor 4, or the proinflammatory cytokines TNF-
, IFN-
, and
IL-1
. These findings, in conjunction with the known immunomodulatory
capacities of PGs, suggest that COX-2 expression by the small intestine
lamina propria is a basal state contributing to the hyporesponsiveness
of the intestinal immune response.
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