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Am J Physiol Endocrinol Metab (February 11, 2002). doi:10.1152/ajpendo.00508.2001
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Articles in PresS, published online ahead of print February 11, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00508.2001
Submitted on November 12, 2001
Accepted on February 7, 2002

Overexpression of CRIP in Transgenic Mice Alters Cytokine Patterns and the Immune Response

Lorraine M Lanningham-Foster1, Calvert L Green1, Bobbi J Langkamp-Henken1, Barbara A Davis1, Khanh T Nguyen1, Bradley S Bender2, and Robert J Cousins1*

1 Food Science and Human Nutrition Department, Center for Nutritional Sciences, University of Florida, Gainesville, FL, USA
2 Department of Medicine, University of Florida, Gainesville, FL, USA; Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center, Gainesville, FL, USA

* To whom correspondence should be addressed. E-mail: RJCousins{at}mail.ifas.ufl.edu.

Cysteine-rich intestinal protein (CRIP5), which contains a double zinc-finger motif, is a member of the Group 2 LIM protein family. Our results showed the developmental regulation of CRIP in neonates was not influenced by conventional vs. specific pathogen free housing conditions. Thymic and splenic CRIP expression was not developmentally regulated. A line of transgenic (Tg) mice which overexpress the rat CRIP gene was created. When challenged with lipopolysaccharide, the Tg mice lost more weight, exhibited increased mortality, experienced greater diarrhea incidence and had less serum IFN-{gamma} and more IL-6 and IL-10. Similarly, splenocytes from the Tg mice produced less IFN-{gamma} and IL-2 and more IL-10 and IL-6 upon mitogen stimulation. Delayed-type hypersensitivity response was less in the Tg mice. Influenza virus infection produced greater weight loss in the Tg mice, which also showed delayed viral clearance. The observed responses to overexpression of the CRIP gene are consistent with a role for this LIM protein in a cellular pathway which produces an imbalance in cytokine pattern favoring Th2 cytokines.




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