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Philadelphia: W.B. Saunders Co., 1999, Proc Natl Acad Sci USA, 2008, 105: 17949, Immunity, 44, 2016, 44: 463, N Engl J Med, 2011, 364: 656). Today, the resolution of inflammation is widely recognized as a cellular biochemically active process involving biosynthesis of a novel superfamily of endogenous chemical signals coined specialized pro\u2010resolving mediators (<jats:styled-content style=\"fixed-case\">SPM<\/jats:styled-content>s; Nature, 2014, 510:92). Herein, we review recent evidence, indicating a role for the vagus nerve and vagotomy in the regulation of lipid mediators. Vagotomy reduces pro\u2010resolving mediators, including the lipoxins, resolvins, protectins and maresins, delaying resolution in mouse peritonitis. Vagotomy also delays resolution of <jats:italic>Escherichia coli<\/jats:italic> infection in mice. Specifically, right vagus regulates peritoneal Group 3 innate lymphoid cell (<jats:styled-content style=\"fixed-case\">ILC<\/jats:styled-content>\u20103) number and peritoneal macrophage responses with lipid mediator profile signatures with elevated pro\u2010inflammatory eicosanoids and reduced resolvins, including the novel protective <jats:italic>immunoresolvent agonist<\/jats:italic> protectin conjugate in tissue regeneration1 (<jats:styled-content style=\"fixed-case\">PCTR<\/jats:styled-content>1). Acetylcholine upregulates <jats:styled-content style=\"fixed-case\">PCTR<\/jats:styled-content> biosynthesis, and administration of <jats:styled-content style=\"fixed-case\">PCTR<\/jats:styled-content>1 to vagotomized mice restores tissue resolution and host responses to <jats:italic>E.\u00a0coli<\/jats:italic> infections. Results obtained with human vagus <jats:italic>ex\u00a0vivo<\/jats:italic> indicate that vagus can produce both pro\u2010inflammatory eicosanoids, such as prostaglandins and leukotrienes, as well as the <jats:styled-content style=\"fixed-case\">SPM<\/jats:styled-content>. Electrical stimulation of human vagus <jats:italic>in\u00a0vitro<\/jats:italic> reduces both prostaglandins and leukotrienes and enhances resolvins and the other <jats:styled-content style=\"fixed-case\">SPM<\/jats:styled-content>. These results elucidate a host protective mechanism mediated by vagus stimulation of <jats:styled-content style=\"fixed-case\">SPM<\/jats:styled-content> that includes resolvins and <jats:styled-content style=\"fixed-case\">PCTR<\/jats:styled-content>1 to regulate myeloid antimicrobial functions and resolution of infection. Moreover, they define a new <jats:italic>pro\u2010resolution of inflammation reflex<\/jats:italic> operative in mice and human tissue that involves a vagus <jats:styled-content style=\"fixed-case\">SPM<\/jats:styled-content> circuit.<\/jats:p>","DOI":"10.1111\/joim.12871","type":"journal-article","created":{"date-parts":[[2018,12,19]],"date-time":"2018-12-19T12:20:52Z","timestamp":1545222052000},"page":"240-258","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":59,"title":["Novel mediators and mechanisms in the resolution of infectious inflammation: evidence for vagus regulation"],"prefix":"10.1111","volume":"286","author":[{"given":"C. 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