{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T19:03:20Z","timestamp":1792782200626,"version":"4.5.0"},"reference-count":35,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2015,8,27]],"date-time":"2015-08-27T00:00:00Z","timestamp":1440633600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"BONFOR","award":["O-112.0053"],"award-info":[{"award-number":["O-112.0053"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2015,10,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The pathophysiology of adhesion formation after abdominal and pelvic surgery is still largely unknown. The aim of the study was to investigate the role of macrophage polarization and the effect of peroxisome proliferator-activated receptor (PPAR) \u03b3 stimulation on adhesion formation in an animal model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Peritoneal adhesion formation was induced by the creation of ischaemic buttons within the peritoneal wall and the formation of a colonic anastomosis in wild-type, interleukin (IL) 10-deficient (IL-10\u2212\/\u2212), IL-4-deficient (IL-4\u2212\/\u2212) and CD11b-Cre\/PPAR\u03b3fl\/fl mice. Adhesions were assessed at regular intervals, and cell preparations were isolated from ischaemic buttons and normal peritoneum. These samples were analysed for macrophage differentiation and its markers, and expression of cytokines by quantitative PCR, fluorescence microscopy, arginase activity and pathological examination. Some animals underwent pioglitazone (PPAR-\u03b3 agonist) or vehicle treatment to inhibit adhesion formation. Anastomotic healing was evaluated by bursting pressure measurement and collagen gene expression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Macrophage M2 marker expression and arginase activity were raised in buttons without adhesions compared with buttons with adhesions. IL-4\u2212\/\u2212 and IL-10\u2212\/\u2212 mice were not affected, whereas CD11b-Cre\/PPAR\u03b3fl\/fl mice showed decreased arginase activity and increased adhesion formation. Perioperative pioglitazone treatment increased arginase activity and decreased adhesion formation in wild-type but not CD11b-Cre\/PPAR\u03b3fl\/fl mice. Pioglitazone had no effect on anastomotic healing.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Endogenous macrophage-specific PPAR-\u03b3 signalling affected arginase activity and macrophage polarization, and counter-regulated peritoneal adhesion manifestation. Pharmacological PPAR-\u03b3 agonism induced a shift towards macrophage M2 polarization and ameliorated adhesion formation in a macrophage-dependent manner.Surgical relevancePostoperative adhesion formation is frequently seen after abdominal surgery and occurs in response to peritoneal trauma. The pathogenesis is still unknown but includes an imbalance in fibrinolysis, collagen production and inflammatory mechanisms. Little is known about the role of macrophages during adhesion formation.In an experimental model, macrophage M2 marker expression was associated with reduced peritoneal adhesion formation and involved PPAR-\u03b3-mediated arginase activity. Macrophage-specific PPAR-\u03b3 deficiency resulted in reduced arginase activity and aggravated adhesion formation. Pioglitazone, a PPAR-\u03b3 agonist, induced M2 polarization and reduced postoperative adhesion formation without compromising anastomotic healing in mice.Pioglitazone ameliorated postoperative adhesion formation without compromising intestinal wound healing. Therefore, perioperative PPAR-\u03b3 agonism might be a promising strategy for prevention of adhesion formation after abdominal surgery.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/bjs.9907","type":"journal-article","created":{"date-parts":[[2015,8,27]],"date-time":"2015-08-27T09:26:23Z","timestamp":1440667583000},"page":"1506-1516","source":"Crossref","is-referenced-by-count":26,"title":["Effects of macrophage-dependent peroxisome proliferator-activated receptor \u03b3 signalling on adhesion formation after abdominal surgery in an experimental model"],"prefix":"10.1093","volume":"102","author":[{"given":"G-S","family":"Hong","sequence":"first","affiliation":[{"name":"Department of Surgery, University Hospital of Bonn, Bonn, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"T","family":"Schwandt","sequence":"additional","affiliation":[{"name":"Department of Surgery, University Hospital of Bonn, Bonn, 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