Interactions between bradykinin (BK) and cell adhesion molecule (CAM) expression in peptidoglycan-polysaccharide (PG-PS)-induced arthritis 1 I. M. SAINZ, A. B. UKNIS, I. ISORDIA-SALAS, R. A. DELA CADENA, R. A. PIXLEY and R. W. COLMAN 2 The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, Pennsylvania, USA 2 Correspondence: The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, 3400 North Broad St., Room 300, OMS, Philadelphia, PA 19140, USA. E-mail: colmanr@temple.edu <h3>SPECIFIC AIM</h3> The aim of this study was to delineate mechanisms by which bradykinin can influence development of chronic synovial inflammation in an animal model of arthritis. We hypothesize that bradykinin can regulate cell adhesion molecules (CAMs) on leukocyte, endothelial, and synovial cells. <h3>PRINCIPAL FINDINGS</h3> 1. Bradykinin-1, bradykinin-2 and combined B1-and-B2 receptor antagonist (B-RA) treatments altered the clinical course of PG-PS-induced arthritis in Lewis rats (Fig. 1) Thirty-three female Lewis rats were separated into five groups: negative control group (HSA; n =4); positive group (PG-PS; n =6); B1-RA ( n =7), B2-RA ( n =8); and combined B1 and B2-RA ( n =8) treatment groups. All groups were followed for 20 days. It was found that 1) B1-RA treatment increased joint swelling; 2)
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