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,
Departments of
* Pediatrics,
Microbiology and Immunology, and
Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD 20814;
Nutritional Requirements and Function Laboratory, Beltsville Human Nutrition and Research Center, Agricultural Research Service, U.S. Department of Agriculture, Beltsville, MD 20705; and
¶ Division of Immunology, Department of Medicine, University of Cincinnati, Cincinnati, OH 45267
Gastrointestinal nematode infections generally invoke a type 2
cytokine response, characterized by the production of IL-4, IL-5, IL-9,
and IL-13. Among these cytokines, IL-4 and IL-13 exhibit a
functional overlap that can be explained by the sharing of a common
receptor or receptor component (IL-4R
). Binding of IL-4 by either
the type 1 or 2 IL-4R, or of IL-13 by the type 2 IL-4R, initiates
Jak-dependent tyrosine phosphorylation of the IL-4R-chain and the
transcription factor, STAT6. In the present study, we investigated: 1)
whether IL-13 has effects on intestinal epithelial cells similar to
those observed with IL-4, and 2) whether the effects of IL-4 and IL-13
depend on STAT6 signaling and/or mast cells. BALB/c,
STAT6-/-, and mast cell-deficient W/Wv mice
or their +/+ littermates were treated with a long-lasting formulation
of recombinant mouse IL-4 (IL-4C) or with IL-13 for seven days.
Segments of jejunum were mounted in Ussing chambers to measure mucosal
permeability; chloride secretion in response to PGE2,
histamine, 5-hydroxytryptamine, or acetylcholine; and
Na+-linked glucose absorption. IL-4C and IL-13 increased
mucosal permeability, decreased glucose absorption, and decreased
chloride secretion in response to 5-hydroxytryptamine. These effects
were dependent on STAT6 signaling. Responses to PGE2 and
histamine, which were dependent on mast cells and STAT6, were enhanced
by IL-4C, but not by IL-13. The effects of IL-4 and IL-13 on intestinal
epithelial cell function may play a critical role in host protection
against gastrointestinal nematodes.
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