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B-mediated expression of iNOS promotes epithelial defense against infection by Cryptosporidium parvum in neonatal piglets
1 Department of Molecular Biomedical Sciences, North Carolina State University College of Veterinary Medicine, Raleigh, NC, USA
2 Department of Veterinary and Biomedical Sciences, University of Minnesota College of Veterinary Medicine, St. Paul, MN, USA
* To whom correspondence should be addressed. E-mail: Jody_Gookin{at}ncsu.edu.
Cryptosporidium sp. parasitizes intestinal epithelium, resulting in enterocyte loss, villous
atrophy, and malabsorptive diarrhea. We have shown that mucosal expression of iNOS is
increased in infected piglets and inhibition of iNOS in vitro has no short-term effect on barrier
function. Nitric oxide exerts inhibitory effects on a variety of pathogens; nevertheless, the
specific sites of iNOS expression, pathways of iNOS induction, and mechanism of NO action in
cryptosporidiosis remain unclear. Here we examined the location, mechanism of induction,
specificity, and consequence of iNOS expression using an in vivo model of C. parvum infection
in neonatal piglets. In acute C. parvum infection, iNOS expression predominated in the villous
epithelium, was NF-
B-dependent, and was not restricted to infected enterocytes. Ongoing
treatment of infected piglets with a selective iNOS inhibitor resulted in significant increases in
villous epithelial parasitism and oocyst excretion but was without detriment to maintenance of
mucosal barrier function. Intensified parasitism could not be attributed to attenuated fluid loss or
changes in epithelial proliferation or replacement rate as iNOS inhibition did not alter severity of
diarrhea, piglet hydration, Cl- secretion or kinetics of BrdU-labeled enterocytes. These findings
suggest that induction of iNOS represents a non-specific response of the epithelium that mediates
enterocyte defense against C. parvum infection. Inducible NOS did not contribute to the
pathogenic sequelae of C. parvum infection.
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