{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T22:46:26Z","timestamp":1790808386470,"version":"4.1.0"},"reference-count":62,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2000,8,7]]},"abstract":"<jats:p>Using intravital microscopy, we examined the role played by B1 receptors in leukocyte trafficking across mouse mesenteric postcapillary venules in vivo. B1 receptor blockade attenuated interleukin (IL)-1\u03b2\u2013induced (5 ng intraperitoneally, 2 h) leukocyte\u2013endothelial cell interactions and leukocyte emigration (\u223c50% reduction). The B1 receptor agonist des-Arg9bradykinin (DABK), although inactive in saline- or IL-8\u2013treated mice, caused marked neutrophil rolling, adhesion, and emigration 24 h after challenge with IL-1\u03b2 (when the cellular response to IL-1\u03b2 had subsided). Reverse transcriptase polymerase chain reaction and Western blot revealed a temporal association between the DABK-induced response and upregulation of mesenteric B1 receptor mRNA and de novo protein expression after IL-1\u03b2 treatment. DABK-induced leukocyte trafficking was antagonized by the B1 receptor antagonist des-arg10HOE 140 but not by the B2 receptor antagonist HOE 140. Similarly, DABK effects were maintained in B2 receptor knockout mice. The DABK-induced responses involved the release of neuropeptides from C fibers, as capsaicin treatment inhibited the responses. Treatment with the neurokinin (NK)1 and NK3 receptor antagonists attenuated the responses, whereas NK2, calcitonin gene-related peptide, or platelet-activating factor receptor antagonists had no effect. Substance P caused leukocyte recruitment that, similar to DABK, was inhibited by NK1 and NK3 receptor blockade. Mast cell depletion using compound 48\/80 reduced DABK-induced leukocyte trafficking, and DABK treatment was shown histologically to induce mast cell degranulation. DABK-induced trafficking was inhibited by histamine H1 receptor blockade. Our findings provide clear evidence that B1 receptors play an important role in the mediation of leukocyte\u2013endothelial cell interactions in postcapillary venules, leading to leukocyte recruitment during an inflammatory response. This involves activation of C fibers and mast cells, release of substance P and histamine, and stimulation of NK1, NK3, and H1 receptors.<\/jats:p>","DOI":"10.1084\/jem.192.3.367","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:48:33Z","timestamp":1027702113000},"page":"367-380","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":96,"title":["Association between Kinin B1 Receptor Expression and Leukocyte Trafficking across Mouse Mesenteric Postcapillary Venules"],"prefix":"10.1084","volume":"192","author":[{"given":"Peter G.","family":"McLean","sequence":"first","affiliation":[{"name":"aDepartment of Biochemical Pharmacology, The William Harvey Research Institute, St. Bartholomew's and the Royal London School of Medicine and Dentistry, London EC1M 6BQ, United Kingdom"},{"name":"bCenter for Clinical Pharmacology, Department of Medicine, University College London, London WC1E 6JJ, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amrita","family":"Ahluwalia","sequence":"additional","affiliation":[{"name":"bCenter for Clinical Pharmacology, Department of Medicine, University College London, London WC1E 6JJ, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mauro","family":"Perretti","sequence":"additional","affiliation":[{"name":"aDepartment of Biochemical Pharmacology, The William Harvey Research Institute, St. Bartholomew's and the Royal London School of Medicine and Dentistry, London EC1M 6BQ, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2000,7,31]]},"reference":[{"key":"2023072509332224400_R1","doi-asserted-by":"crossref","first-page":"100","DOI":"10.1016\/S0165-6147(99)01321-8","article-title":"B1 receptors as a new inflammatory target","volume":"20","author":"Ahluwalia","year":"1999","journal-title":"Trends Pharmacol. 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