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The aim of the present study was to investigate the role of M2 Arg-1<jats:sup>+<\/jats:sup> M\u0424 in tuberculous pleurisy-assisted tumorigenicity in vitro and in vivo.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>The interactions between tuberculous pleural effusion (TPE)-induced M2 Arg-1<jats:sup>+<\/jats:sup> M\u0424 and A549 lung cancer cells were evaluated. A murine model injected with cancer cells 2\u00a0weeks after <jats:italic>Mycobacterium bovis<\/jats:italic> bacillus Calmette\u2013Gu\u00e9rin pleural infection was used to validate the involvement of tuberculous fibrosis to tumor invasion.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Increased CXCL9 and CXCL10 levels of TPE induced M2 Arg-1<jats:sup>+<\/jats:sup> M\u0424 polarization of murine bone marrow-derived M\u0424. TPE-induced M2 Arg-1<jats:sup>+<\/jats:sup> M\u0424 polarization facilitated lung cancer proliferation via autophagy signaling and E-cadherin signaling in vitro. An inhibitor of arginase-1 targeting M2 Arg-1<jats:sup>+<\/jats:sup> M\u0424 both in vitro and in vivo significantly reduced tuberculous fibrosis-induced metastatic potential of lung cancer and decreased autophagy signaling and E-cadherin expression.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Tuberculous pleural fibrosis induces M2 Arg-1<jats:sup>+<\/jats:sup> polarization, and M2 Arg-1<jats:sup>+<\/jats:sup> M\u0424 contribute to lung cancer metastasis via autophagy and E-cadherin signaling. Therefore, M2 Arg-1<jats:sup>+<\/jats:sup> tumor associated M\u0424 may be a novel therapeutic target for tuberculous fibrosis-induced lung cancer progression.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12931-024-02829-8","type":"journal-article","created":{"date-parts":[[2024,5,8]],"date-time":"2024-05-08T09:02:40Z","timestamp":1715158960000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Tuberculous pleural effusion-induced Arg-1+ macrophage polarization contributes to lung cancer progression via autophagy signaling"],"prefix":"10.1186","volume":"25","author":[{"given":"Seong Ji","family":"Woo","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Youngmi","family":"Kim","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hyun-Jung","family":"Kang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harry","family":"Jung","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dong Hyuk","family":"Youn","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoonki","family":"Hong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jae Jun","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ji Young","family":"Hong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,5,8]]},"reference":[{"issue":"3","key":"2829_CR1","doi-asserted-by":"publisher","first-page":"765","DOI":"10.3390\/jcm11030765","volume":"11","author":"SY Hwang","year":"2022","unstructured":"Hwang SY, Kim JY, Lee HS, Lee S, Kim D, Kim S, Hyun JH, Shin JI, Lee KH, Han SH, Song YG. 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