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/CCL20 production by human
intestinal epithelium: mechanism for modulating mucosal immunity
Laboratory of Mucosal Immunology, Department of Medicine, University of California, San Diego, La Jolla, California 92093-0623
Human intestinal
epithelial cells secrete an array of chemokines known to signal the
trafficking of neutrophils and monocytes important in innate mucosal
immunity. We hypothesized that intestinal epithelium may also have the
capacity to play a role in signaling host adaptive immunity. The CC
chemokine macrophage inflammatory protein (MIP)-3
/CCL20 is
chemotactic for immature dendritic cells and CD45RO+ T
cells that are important components of the host adaptive immune system.
In these studies, we demonstrate the widespread production and
regulated expression of MIP-3 by human intestinal epithelium. Several intestinal epithelial cell lines were shown to constitutively express MIP-3 mRNA. Moreover, MIP-3 mRNA expression and protein production were upregulated by stimulation of intestinal epithelial cells with the proinflammatory cytokines tumor necrosis factor- or
interleukin-1 or in response to infection with the enteric bacterial
pathogens Salmonella or enteroinvasive Escherichia
coli. In addition, MIP-3 was shown to function as a nuclear
factor-
B target gene. In vitro findings were paralleled in vivo by
increased expression of MIP-3 in the epithelium of
cytokine-stimulated or bacteria-infected human intestinal xenografts
and in the epithelium of inflamed human colon. Mucosal T cells, other
mucosal mononuclear cells, and intestinal epithelial cells expressed
CCR6, the cognate receptor for MIP-3. The constitutive and regulated
expression of MIP-3 by human intestinal epithelium is consistent
with a role for epithelial cell-produced MIP-3 in modulating mucosal adaptive immune responses.
chemokines; dendritic cells; infectious immunity; inflammation; T lymphocytes
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