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*
Intestinal Disease Research Program, McMaster University, Hamilton, Ontario, Canada; and
Neuroscience and Gastrointestinal Research Groups, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
Bacterial superantigens (SAgs) are potent T cell activators. Mice
treated 4 h previously with the SAg, Staphylococcus
aureus enterotoxin B (SEB), display reduced ion transport
(assessed by short circuit current) responses to prosecretory stimuli,
which normalize 24 h posttreatment. Here, mice were treated with
SEB alone or in combination with an inhibitor of the inducible form of
NO synthase (iNOS), L-NIL. Subsequently, jejunal iNOS
expression was detected by immunohistochemistry, ion transport was
evaluated in Ussing chambers, and serum levels of TNF-
and IFN-
were measured by ELISA. SEB-treated mice had increased epithelial iNOS
immunoreactivity, and numerous iNOS-positive CD3+ T cells
occurred in their mucosa and submucosa. Concomitant treatment with
L-NIL did not affect the reduced short circuit current
responsiveness to electrical nerve stimulation or the prosecretory
agents, carbachol and forskolin, that occurred 4 h post-SEB (5
µg) treatment. However, Isc responses in L-NIL- plus
SEB-treated mice were still significantly reduced 24 h
posttreatment, indicating a role for NO in the restoration of normal
ion transport following exposure to SAgs. The prolongation of
epithelial ion transport abnormalities correlated with elevated serum
levels of TNF- and IFN- in mice treated 24 h previously with
L-NIL plus SEB compared with those in controls and
SEB-only-treated mice. Additionally, mice treated with
L-NIL plus SEB and TNF-- or IFN--neutralizing Abs
displayed normal jejunal ion transport characteristics 24 h
posttreatment. We conclude that NO mobilization is important in the
homeostatic recovery response following immune stimulation by SAgs and
that the beneficial effect of NO in this model system is probably via
regulation of TNF- and IFN- production.
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