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Intestinal Disease Research Program, Departments of 1 Pathology and Molecular Medicine and 2 Medicine, McMaster University, Hamilton, Ontario, Canada L8P 3Z5
Increased epithelial permeability is associated with intestinal
inflammation, but there is little information on factors that regulate
barrier function in the absence of or before inflammation. We examined
if interleukin (IL)-4, or serum from atopic individuals, could alter
the barrier function of human colonic epithelial (T84) monolayers to
antigenic-sized macromolecules. IL-4 and atopic serum significantly
decreased T84 monolayer resistance and increased transepithelial
horseradish peroxidase (HRP) transport. Bidirectional transport studies
demonstrated that IL-4 selectively enhanced apical-to-basal movement of
HRP. HRP transport induced by IL-4 was inhibited by cold (4°C) and
the tyrosine kinase inhibitor genistein, but not the protein kinase C
inhibitor staurosporine. Electron microscopic analysis demonstrated
that both transcellular and paracellular pathways were affected.
Anti-IL-4 antibodies abolished the increase in HRP transport in
response to both IL-4 and serum. We speculate that enhanced production
of IL-4 in allergic conditions may be a predisposing factor to
inflammation by allowing uptake of luminal antigens that gain access to
the mucosal immune system.
transcytosis; paracellular; allergy; inflammation; interleukin-4
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