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Inhibition of IFN--Inducible Protein-10 Abrogates Colitis in IL-10^-/- Mice ¹

Udai P. Singh^*, Shailesh Singh^*, Dennis D. Taub and James W. Lillard, Jr.^2,*

^* Department of Microbiology and Immunology, Morehouse School of Medicine, Atlanta, GA 30310; and Laboratory of Immunology, National Institute on Aging, Gerontology Research Center, Baltimore, MD 21224

A deficiency in understanding the steps responsible for colitis is the lack of comprehension for the role chemokines play in mucosal inflammation. IFN--inducible protein-10 (IP-10) and CXCR3 are highly expressed at sites of colitis. Our findings show that IP-10 significantly contributes to the development of Th1 and inflammatory responses. Specifically, IP-10 inhibition in IL-10^-/- mice attenuates the associated increases in serum and/or local amyloid A, IL-2, IL-6, TNF-, IFN-, IL-1, and IL-1 with colitis as compared with IL-10^-/- mice that develop colitis similar to human Crohn’s disease. Correspondingly, the rate or intensity of inflammation in IL-10^-/- mice treated with anti-IP-10 Abs showed improved scoring of inflammation, compared with control IL-10^-/- mice. This study provides important and novel information regarding IP-10 as a target for the treatment of colitis.

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