{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T01:02:58Z","timestamp":1792112578657,"version":"4.4.0"},"reference-count":41,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1998,3,1]],"date-time":"1998-03-01T00:00:00Z","timestamp":888710400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["faseb.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The FASEB Journal"],"published-print":{"date-parts":[[1998,3]]},"abstract":"<jats:p>\n                    The kallikrein\u2010kinin (K\u2010K) (contact) system is activated during acute and chronic relapsing phases of enterocolitis induced in genetically susceptible Lewis rats by intramural injection of peptidogly\u2010can\u2010polysaccharide (PG\u2010APS). Using the selective plasma kallikrein inhibitor P8720, we investigate whether activation of the K\u2010K system plays a primary role in chronic granulomatous intestinal and systemic inflammation in this model. Group I (negative control) received human serum albumin intramurally. Group II (treatment) received PG\u2010APS intramurally and P8720 orally. Group III (positive control) received PG\u2010APS intramurally and albumin orally. P8720 attenuated the consumption of the contact proteins, high molecular weight kininogen (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.03), and factor XI (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.04) in group II vs. group III. P8720 decreased chronic intestinal inflammation measured by blinded gross (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01) and histologic (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.0005) scores as well as systemic complications (arthritis, splenomegaly, hepatomegaly, leukocytosis, and acute\u2010phase reaction) (\n                    <jats:italic>P<\/jats:italic>\n                    &lt; 0.01) in group II as compared with group III. We conclude that relapsing chronic enterocolitis and systemic complications are in part due to plasma K\u2010K system activation, and that inhibition of this pathway is a potential therapeutic approach to human inflammatory bowel disease and associated extraintestinal manifestations.\u2014Stadnicki, A., Sartor, R. B., Janardham, R., Majluf\u2010Cruz, A., Kettner, C. A., Adam, A. A., Colman, R. W. Specific inhibition of plasma kallikrein modulates chronic granulomatous intestinal and systemic inflammation in genetically susceptible rats.\n                    <jats:italic>FASEB J.<\/jats:italic>\n                    12, 325\u2013333 (1998)\n                  <\/jats:p>","DOI":"10.1096\/fasebj.12.3.325","type":"journal-article","created":{"date-parts":[[2018,1,25]],"date-time":"2018-01-25T04:40:58Z","timestamp":1516855258000},"page":"325-333","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":37,"title":["Specific inhibition of plasma kallikrein modulates chronic granulomatous intestinal and systemic inflammation in genetically susceptible rats"],"prefix":"10.1096","volume":"12","author":[{"given":"Antoni","family":"Stadnicki","sequence":"first","affiliation":[{"name":"Sol Sherry Thrombosis Research Center Temple University School of Medicine  Philadelphia 19140 Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R. Balfour","family":"Sartor","sequence":"additional","affiliation":[{"name":"Center for Gastrointestinal Biology and Diseases University of North Carolina  Chapel Hill 27599 North Carolina USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ram","family":"Janardham","sequence":"additional","affiliation":[{"name":"Center for Gastrointestinal Biology and Diseases University of North Carolina  Chapel Hill 27599 North Carolina USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abraham","family":"Majluf\u2010CRUZ","sequence":"additional","affiliation":[{"name":"Sol Sherry Thrombosis Research Center Temple University School of Medicine  Philadelphia 19140 Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles A.","family":"Kettner","sequence":"additional","affiliation":[{"name":"DuPont Merck Pharmaceutical Company  Wilmington 19880\u20130500 Delaware USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Albert A.","family":"Adam","sequence":"additional","affiliation":[{"name":"Department of Pharmacy University of Montreal  Montreal Quebec H3C 3J7 Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert W.","family":"Colman","sequence":"additional","affiliation":[{"name":"Sol Sherry Thrombosis Research Center Temple University School of Medicine  Philadelphia 19140 Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1998,3]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199109263251306"},{"key":"e_1_2_6_3_1","doi-asserted-by":"crossref","first-page":"475","DOI":"10.1016\/S0889-8553(21)00207-7","article-title":"Current concepts of the etiology and pathogenesis of ulcerative colitis and Crohn's disease.","volume":"24","author":"Sartor R. 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