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1 Infectious Disease and
2 Nephrology Sections, Department
of Medicine, Veterans Affairs Medical Center, University of Minnesota
School of Medicine, Minneapolis, Minnesota 55417;
3 Naval Medical Research Institute
Detachment,
Vibrio cholerae induces massive
intestinal fluid secretion that continues for the life of the
stimulated epithelial cells. Enhanced regional blood flow and
peristalsis are required to adapt to this obligatory intestinal
secretory challenge. Nitric oxide (NO) is a multifunctional molecule
that modulates blood flow and peristalsis and possesses both cytotoxic
and antibacterial activity. We demonstrate that, compared with those in
asymptomatic control subjects, levels of stable NO metabolites
(
/
) are significantly increased in sera from acutely ill Peruvian patients
with natural cholera infection as well as from symptomatic volunteers
from the United States infected experimentally with V. cholerae. In a rabbit ileal loop model in vivo, cholera
toxin (CT) elicited fluid secretion and dose-dependent increases in levels of
/
in the fluid (P < 0.01). In
contrast, lipopolysaccharide (LPS) elicited no such effects when
applied to the intact mucosa. NO synthase (NOS) catalytic activity also
increased in toxin-exposed tissues (P < 0.05), predominantly in epithelial cells. The CT-induced NOS activity was Ca2+ dependent and
was not suppressed by dexamethasone. In conclusion, symptomatic
V. cholerae infection induces NO
production in humans. In the related animal model, CT, but not LPS,
stimulated significant production of NO in association with increases
in local Ca2+-dependent NOS
activity in the tissues.
epithelial cells; mucosal response to infection; innate intestinal immunity
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