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From the Intestinal Disease Research Program,*
McMaster
University, Hamilton; and the Division of Gastroenterology and
Nutrition,
Research Institute, The Hospital
for Sick Children, University of Toronto, Toronto, Ontario, Canada
Intestinal immune cells are less reactive than those in the
peripheral blood; however, such cells from patients with
Crohn’s disease may be more responsive to bacterial products. Our
study examined if nonpathogenic bacteria or lipopolysaccharide
(LPS), can affect epithelial function in the presence of
monocytes/macrophages. Lamina propria mononuclear cells (LPMCs) and
peripheral blood monocytes (PBMs) were obtained from patients with
Crohn’s disease and control patients. Filter-grown T84 epithelial
monolayers were co-cultured with nonactivated or LPS-activated LPMCs or
PBMs for 48 hours. Epithelial secretory [baseline short-circuit
current (Isc) and 
Isc to forskolin] and barrier (transepithelial
electrical resistance) parameters were measured in Ussing chambers.
LPS-activated PBMs from both controls and patients with Crohn’s
disease significantly increased Isc (
300%) and reduced
transepithelial electrical resistance (40%). Epithelial function
was not altered after co-culture with control LPMCs ± LPS.
However, LPMCs from patients with Crohn’s disease
spontaneously secreted tumor necrosis factor-
, and induced
epithelial changes similar to those produced by LPS-activated PBMs.
Co-culture with control Escherichia coli and PBMs
induced comparable changes in epithelial physiology, which were
abrogated by anti-tumor necrosis factor- antibody. We conclude that
LPMCs of patients with Crohn’s disease are spontaneously
activated, possibly by gram-negative luminal bacteria,
and can directly cause significant alterations in epithelial ion
transport and barrier functions.
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