{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T18:30:19Z","timestamp":1793212219681,"version":"4.5.0"},"reference-count":39,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation"],"published-print":{"date-parts":[[2021,9,14]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Cardiovascular diseases and chronic kidney disease (CKD) are highly prevalent, aggravate each other, and account for substantial mortality. Both conditions are characterized by activation of the innate immune system. The alarmin interleukin-1\u03b1 (IL-1\u03b1) is expressed in a variety of cell types promoting (sterile) systemic inflammation. The aim of the present study was to examine the role of IL-1\u03b1 in mediating inflammation in the setting of acute myocardial infarction (AMI) and CKD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      We assessed the expression of IL-1\u03b1 on the surface of monocytes from patients with AMI and patients with CKD and determined its association with atherosclerotic cardiovascular disease events during follow-up in an explorative clinical study. Furthermore, we assessed the inflammatory effects of IL-1\u03b1 in several organ injury models in\n                      <jats:italic>Il1a<\/jats:italic>\n                      <jats:sup>\u2212\/<\/jats:sup>\n                      <jats:sup>\u2212<\/jats:sup>\n                      and\n                      <jats:italic>Il1b<\/jats:italic>\n                      <jats:sup>\u2212\/<\/jats:sup>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice and investigated the underlying mechanisms in vitro in monocytes and endothelial cells.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>IL-1\u03b1 is strongly expressed on the surface of monocytes from patients with AMI and CKD compared with healthy controls. Higher IL-1\u03b1 surface expression on monocytes from patients with AMI and CKD was associated with a higher risk for atherosclerotic cardiovascular disease events, which underlines the clinical relevance of IL-1\u03b1. In mice, IL-1\u03b1, but not IL-1\u03b2, mediates leukocyte-endothelial adhesion as determined by intravital microscopy. IL-1\u03b1 promotes accumulation of macrophages and neutrophils in inflamed tissue in vivo. Furthermore, IL-1\u03b1 on monocytes stimulates their homing at sites of vascular injury. A variety of stimuli such as free fatty acids or oxalate crystals induce IL-1\u03b1 surface expression and release by monocytes, which then mediates their adhesion to the endothelium via IL-1 receptor-1. IL-1\u03b1 also promotes expression of the VCAM-1 (vascular cell adhesion molecule-1) on endothelial cells, thereby fostering the adhesion of circulating leukocytes. IL-1\u03b1 induces inflammatory injury after experimental AMI, and abrogation of IL-1\u03b1 prevents the development of CKD in oxalate or adenine-fed mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions:<\/jats:title>\n                    <jats:p>IL-1\u03b1 represents a key mediator of leukocyte-endothelial adhesion and inflammation in AMI and CKD. Inhibition of IL-1\u03b1 may serve as a novel anti-inflammatory treatment strategy.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/circulationaha.121.053547","type":"journal-article","created":{"date-parts":[[2021,7,1]],"date-time":"2021-07-01T05:02:54Z","timestamp":1625115774000},"page":"893-908","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":99,"title":["Interleukin-1\u03b1 Is a Central Regulator of Leukocyte-Endothelial Adhesion in Myocardial Infarction and in Chronic Kidney Disease"],"prefix":"10.1161","volume":"144","author":[{"given":"Stefan J.","family":"Schunk","sequence":"first","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Triem","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."},{"name":"Translational Cardiorenal Medicine (S.T., E.B., G.H., F.K., T. Speer), Saarland University, Homburg\/Saar, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David","family":"Schmit","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen","family":"Zewinger","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamim","family":"Sarakpi","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ellen","family":"Becker","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."},{"name":"Translational Cardiorenal Medicine (S.T., E.B., G.H., F.K., T. Speer), Saarland University, Homburg\/Saar, Germany."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregor","family":"H\u00fctter","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine IV, Nephrology and Hypertension (S.J.S., S.T., D.S., S.Z., T. Sarakpi, E.B., G.H., F.K., D.F., T. Speer), Saarland University, Homburg\/Saar, Germany."},{"name":"Translational Cardiorenal Medicine (S.T., E.B., G.H., F.K., T. 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