{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T02:01:04Z","timestamp":1792807264674,"version":"4.5.0"},"reference-count":29,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T00:00:00Z","timestamp":1768348800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T00:00:00Z","timestamp":1770336000000},"content-version":"vor","delay-in-days":23,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Sci Rep"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The \u03b17 nicotinic acetylcholine receptor (\u03b17nAChR) on macrophages exerts anti-inflammatory effects by suppressing the JAK\/STAT and NF-\u03baB pathways. Although the role of \u03b17nAChR in immunoregulatory mechanisms in \u201cindividual\u201d macrophages is established, studies on \u03b17nAChR in an \u201coverall population\u201d of macrophages, including M1\/M2 polarity, remain limited. Therefore, we examined the role of \u03b17nAChR in M1\/M2 polarity in inflammation. We generated peritonitis mouse models via LPS treatment and sterile intestinal manipulation in wild-type and \u03b17nAChR-deficient mice. M1\/M2 macrophage polarization was measured using PCR and flow cytometry. THP-1 and human peripheral blood mononuclear cells (hPBMC)-derived monocytes were treated with the \u03b17nAChR agonist PNU-282987 during differentiation into M1\/M2 macrophages. \u03b17nAChR deficiency upregulated mRNA expression of the M1 marker and downregulated the M2 marker in a peritoneal cell population. Flow cytometry analysis revealed that the proportion of M2 macrophages in the peritoneal cell population decreased in \u03b17nAChR-deficient mice in both models. In splenectomized LPS-treated wild-type mice, the proportion of M2 macrophages in the peritoneal cell population was reduced compared to that in sham-operated LPS-treated mice. The M2 marker\n                    <jats:italic>CD206<\/jats:italic>\n                    and\n                    <jats:italic>IL10<\/jats:italic>\n                    were upregulated in PNU-282987-treated THP-1 and hPBMC-derived macrophages. These results revealed that \u03b17nAChR exerted M2-enhancing effects with the mechanism suggestively acting in the spleen.\n                  <\/jats:p>","DOI":"10.1038\/s41598-026-35757-2","type":"journal-article","created":{"date-parts":[[2026,1,14]],"date-time":"2026-01-14T07:17:16Z","timestamp":1768375036000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The role of the \u03b17 nicotinic acetylcholine receptor in promoting M2 macrophage polarization at inflammatory sites"],"prefix":"10.1038","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0009-0003-1611-8329","authenticated-orcid":false,"given":"Taiki","family":"Mihara","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hiroshi","family":"Tanabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuma","family":"Nonoshita","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuki","family":"Yamakawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tamaki","family":"Kurosawa","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masatoshi","family":"Hori","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,1,14]]},"reference":[{"key":"35757_CR1","doi-asserted-by":"publisher","first-page":"6166","DOI":"10.4049\/jimmunol.164.12.6166","volume":"164","author":"CD Mills","year":"2000","unstructured":"Mills, C. 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