Novel IBD therapeutic approaches reported from Washington Univ., Barcelona, LSU at A...( imental colitis. This was prompted by t...)

imental colitis. This was prompted by the recognition of cross-talk between platelets and leukocytes in inflammation. Compared with controls, colitis-induced wild type mice showed significantly increased adhesion of platelets, with 2.5% of platelets adhering to ECs directly and 97.5% binding to adherent WBC. ICAM-1 deficient mice with induced colitis had significantly decreased platelet-WBC adhesion.

Wild-type mice made neutropenic with anti-netrophil serum (ANS) exhibited reduced platelet-WBC binding, but significantly increased platelet-EC adhesion. The increase in platelet-EC adhesion in neutropenic animals was presented by both, a single dose of either P-selectin of PSGL-1 blocking monoclonal antibody.

They conclude that in induced colitis, platelet accumulation in venules is dependent on both leukocyte adhesion as well as on mechanisms involving the adhesion molecules P-selectin and PSGL-1. The researchers from the Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, include Thorsten Vowinkel, Mikiji Mori, Katherine Wood, Janice Russel and D. Neil Granger; and Christian F. Krieglstein from the Department of General Surgery, University of Muenster, Germany.

CTLA-4-Ig abrogates TNBS colitis

Researchers at the Division of Gastroenterology of Washington University School of Medicine, St. Louis, Mo., wanted to determine if the biological agent CTLA-4-Ig would abrogate trinitrobenzene sulfonic acid (TNBS) colitis, and if so, to determine if indoleamine 2,3-dioxygenase (IDO) played a role in the process.

The researchers included Gregory J. Gurtner, Thomas M. Ogel, Suzanne R. Schloemann, Keely G. McDonald, Rodney D. Newberry and William F. Stenson.

They found that CTLA-4-Ig induced IDO in the murine colon after systemic administration.

Intraperitonial CTLA-4-Ig administration prior to TNBS administration significantly a
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Contact: Mayer Resnick
mresnick@the-aps.org
301-634-7209
American Physiological Society
9-Sep-2004


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