{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T04:38:34Z","timestamp":1776919114004,"version":"3.51.2"},"reference-count":97,"publisher":"MDPI AG","issue":"22","license":[{"start":{"date-parts":[[2021,11,9]],"date-time":"2021-11-09T00:00:00Z","timestamp":1636416000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"University of Otago Vice-Chancellor\u2019s Strategic Development Fund","award":["-"],"award-info":[{"award-number":["-"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Inflammation is a natural response to tissue injury. Uncontrolled inflammatory response leads to inflammatory disease. Acute pancreatitis is one of the main reasons for hospitalization amongst gastrointestinal disorders worldwide. It has been demonstrated that endogenous hydrogen sulfide (H2S), a gasotransmitter and substance P, a neuropeptide, are involved in the inflammatory process in acute pancreatitis. Cell adhesion molecules (CAM) are key players in inflammatory disease. Immunoglobulin (Ig) gene superfamily, selectins, and integrins are involved at different steps of leukocyte migration from blood to the site of injury. When the endothelial cells get activated, the CAMs are upregulated which leads to them interacting with leukocytes. This review summarizes our current understanding of the roles H2S, substance P and adhesion molecules play in acute pancreatitis.<\/jats:p>","DOI":"10.3390\/ijms222212136","type":"journal-article","created":{"date-parts":[[2021,11,9]],"date-time":"2021-11-09T21:39:07Z","timestamp":1636493947000},"page":"12136","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Role of Hydrogen Sulfide, Substance P and Adhesion Molecules in Acute Pancreatitis"],"prefix":"10.3390","volume":"22","author":[{"given":"Ayush","family":"Kumar","sequence":"first","affiliation":[{"name":"Department of Pathology and Biomedical Science, University of Otago, Christchurch 8140, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Madhav","family":"Bhatia","sequence":"additional","affiliation":[{"name":"Department of Pathology and Biomedical Science, University of Otago, Christchurch 8140, New Zealand"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1968","published-online":{"date-parts":[[2021,11,9]]},"reference":[{"key":"ref_1","unstructured":"Kumar, V., Abbas, A., Aster, J., Turner, J., Perkins, J., and Robbins, S. 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