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Am J Physiol Gastrointest Liver Physiol (March 6, 2002). doi:10.1152/ajpgi.00514.2001
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Articles in PresS, published online ahead of print March 6, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00514.2001
Submitted on December 4, 2001
Accepted on February 4, 2002

Kininogen (HK) Deficiency Modulates Chronic Intestinal Inflammation in Genetically Susceptible Rats

Irma Isordia-Salas1, Robin A Pixley1, Fengling Li2, Irma Sainz1, R Balfour Sartor2, Albert Adam3, and Robert W Colman1*

1 The Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia, PA, USA
2 Department of Medicine, University of North Carolina, Chapel Hill, NC, USA
3 Department of Pharmacology, University of Montreal, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: robert.colman{at}temple.edu.

Genetically susceptible Lewis rats injected in the intestinal wall with peptidoglycanpolysaccharide (PG-APS) polymers develop chronic granulomatous enterocolitis concomitant with activation of the kallikrein-kinin system. To elucidate the role of high molecular weight kininogen (HK) in chronic enterocolitis, we backcrossed Brown-Norway rats having a HK deficiency with Lewis rats for 5 generations. Two new strains were produced, wild type F5 (F5WT) and HK deficient (F5HKd), each with a ~97% Lewis genome. The HK values of F5WT rat plasma and F5HKd rat plasma were 0.62±0.20 units/ml and 0.08±0.03 unit/ml respectively. In PG-APS injected rats, chronic inflammation was measured using gross gut score, histologic inflammation, liver granuloma and white blood cell count. The mean gross gut scores were significantly lower in the F5HKd than the F5WT rats. Plasma T-kininogen was significantly less in F5HKd. These results indicate the importance of the kallikrein-kinin system in this model of chronic enterocolitis and systemic inflammation.






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