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Departments of 1 Molecular and Cellular Physiology and 2 Microbiology and Immunology, Louisiana State University Medical Center, Shreveport, Louisiana 71130
The objectives of this study
were to assess the role of the inducible isoform of nitric oxide
synthase (iNOS) on vascular cell adhesion molecule 1 (VCAM-1)
expression in vivo in an acute model of inflammation induced in
iNOS-deficient
(iNOS
/) mice and
compare these data to those obtained by pharmacological inhibition of
iNOS in a CD4+ T
lymphocyte-dependent model of chronic colitis. VCAM-1 expression was
quantified in vivo using the dual radiolabel monoclonal antibody technique. We found that intraperitoneal injection of 10 µg/kg tumor
necrosis factor-
(TNF-) enhanced VCAM-1 expression by approximately twofold in the colon, cecum, and stomach but not small
intestine in iNOS/
mice compared with TNF--injected wild-type mice. Injection of wild-type mice with 25 µg/kg TNF- further enhanced VCAM-1
expression by approximately twofold compared with wild-type mice
injected with 10 µg/kg TNF-; however, VCAM-1 expression was not
further enhanced in any gastrointestinal organ system in
iNOS/ mice. In a
second series of experiments, we found that continuous inhibition of
iNOS using oral administration of
NG-iminoethyl-L-lysine
did not alter the enhanced levels of VCAM-1 expression in the colon nor
did it alter the severity of colonic inflammation in SCID mice
reconstituted with CD4+,
CD45RBhigh T cells. We conclude
that iNOS may regulate VCAM-1 expression in acute inflammation;
however, this effect is modest and tissue specific and occurs only when
VCAM-1 expression is submaximal. iNOS does not appear to modulate
VCAM-1 expression in an immune model of chronic colitis.
neutrophils; nuclear factor-
B; endothelium
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