{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T22:37:39Z","timestamp":1793227059678,"version":"4.5.0"},"reference-count":51,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2021,12,1]],"date-time":"2021-12-01T00:00:00Z","timestamp":1638316800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/100000062","name":"HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases","doi-asserted-by":"publisher","award":["ARS Project 8050-51000-097-02S"],"award-info":[{"award-number":["ARS Project 8050-51000-097-02S"]}],"id":[{"id":"10.13039\/100000062","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute","doi-asserted-by":"publisher","award":["RO1HL106173"],"award-info":[{"award-number":["RO1HL106173"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>In response to infection or tissue damage, resident peritoneal macrophages (rpMACs) produce inflammatory lipid mediators from the polyunsaturated fatty acid (PUFA), arachidonic acid (AA). Long-chain acyl-CoA synthetase 4 (ACSL4) catalyzes the covalent addition of a CoA moiety to fatty acids, with a strong preference for AA and other PUFAs containing three or more double bonds. PUFA-CoA can be incorporated into phospholipids, which is the source of PUFA for lipid mediator synthesis. In this study, we demonstrated that deficiency of Acsl4 in mouse rpMACs resulted in a significant reduction of AA incorporated into all phospholipid classes and a reciprocal increase in incorporation of oleic acid and linoleic acid. After stimulation with opsonized zymosan (opZym), a diverse array of AA-derived lipid mediators, including leukotrienes, PGs, hydroxyeicosatetraenoic acids, and lipoxins, were produced and were significantly reduced in Acsl4-deficient rpMACs. The Acsl4-deficient rpMACs stimulated with opZym also demonstrated an acute reduction in mRNA expression of the inflammatory cytokines, Il6, Ccl2, Nos2, and Ccl5. When Acsl4-deficient rpMACs were incubated in vitro with the TLR4 agonist, LPS, the levels of leukotriene B4 and PGE2 were also significantly decreased. In LPS-induced peritonitis, mice with myeloid-specific Acsl4 deficiency had a significant reduction in leukotriene B4 and PGE2 levels in peritoneal exudates, which was coupled with reduced infiltration of neutrophils in the peritoneal cavity as compared with wild-type mice. Our data demonstrate that chronic deficiency of Acsl4 in rpMACs reduces the incorporation of AA into phospholipids, which reduces lipid mediator synthesis and inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.2100393","type":"journal-article","created":{"date-parts":[[2021,11,1]],"date-time":"2021-11-01T12:35:16Z","timestamp":1635770116000},"page":"2744-2753","source":"Crossref","is-referenced-by-count":31,"title":["Myeloid-Specific Deficiency of\n                    <i>Long-Chain Acyl CoA Synthetase 4<\/i>\n                    Reduces Inflammation by Remodeling Phospholipids and Reducing Production of Arachidonic Acid\u2013Derived Proinflammatory Lipid Mediators"],"prefix":"10.1093","volume":"207","author":[{"given":"Andrew R","family":"Reeves","sequence":"first","affiliation":[{"name":"Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University , Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6339-2940","authenticated-orcid":false,"given":"Brian E","family":"Sansbury","sequence":"additional","affiliation":[{"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5697-6086","authenticated-orcid":false,"given":"Meixia","family":"Pan","sequence":"additional","affiliation":[{"name":"Barshop Institute for Longevity and Aging Research, University of Texas Health Science Center at San Antonio , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8615-2413","authenticated-orcid":false,"given":"Xianlin","family":"Han","sequence":"additional","affiliation":[{"name":"Barshop Institute for Longevity and Aging Research, University of Texas Health Science Center at San Antonio , San Antonio, TX"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8868-3648","authenticated-orcid":false,"given":"Matthew","family":"Spite","sequence":"additional","affiliation":[{"name":"Center for Experimental Therapeutics and Reperfusion Injury, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women\u2019s Hospital and Harvard Medical School , Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5062-387X","authenticated-orcid":false,"given":"Andrew S","family":"Greenberg","sequence":"additional","affiliation":[{"name":"Jean Mayer USDA Human Nutrition Research Center on Aging, Tufts University , Boston, MA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2021,12,1]]},"reference":[{"key":"2025022610323123300_r1","doi-asserted-by":"crossref","first-page":"986","DOI":"10.1038\/ni.2705","article-title":"Tissue-resident macrophages","volume":"14","author":"Davies","year":"2013","journal-title":"Nat. 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