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Vagal \u03b17nAChR signaling plays a key role in regulating lung infection and inflammation; however, whether this pathway regulates \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>cells during lung injury repair remains unknown. We hypothesized that vagal \u03b17nAChR signaling controls \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>cells, which contribute to the resolution of lung injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Pneumonia was induced by intratracheal challenge with<jats:italic>E. coli<\/jats:italic>. The bone marrow mononuclear cells (BM-MNCs) were isolated from the bone marrow of pneumonia mice for immunofluorescence. The bone marrow, blood, BAL, and lung cells were isolated for flow cytometric analysis by labeling with anti-Sca1, VE-cadherin, p-Akt1, or Flk1 antibodies. Immunofluorescence was also used to examine the coexpression of \u03b17nAChR, VE-cadherin, and p-Akt1. Sham, vagotomized, \u03b17nAChR knockout, and Akt1 knockout mice were infected with<jats:italic>E. coli<\/jats:italic>to study the regulatory role of vagal \u03b17nAChR signaling and Akt1 in Sca1<jats:sup>+<\/jats:sup>cells.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>During pneumonia, BM-MNCs were enriched with \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>cells, and this cell population proliferated. Transplantation of pneumonia BM-MNCs could mitigate lung injury and increase engraftment in recipient pneumonia lungs. Activation of \u03b17nAChR by its agonist could boost \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>cells in the bone marrow, peripheral blood, and bronchoalveolar lavage (BAL) in pneumonia. Immunofluorescence revealed that \u03b17nAChR, VE-cadherin, and p-Akt1 were coexpressed in the bone marrow cells. Vagotomy could reduce \u03b17nAChR<jats:sup>+<\/jats:sup>VE-cadherin<jats:sup>+<\/jats:sup>and VE-cadherin<jats:sup>+<\/jats:sup>p-Akt1<jats:sup>+<\/jats:sup>cells in the bone marrow in pneumonia. Knockout of \u03b17nAChR reduced VE-cadherin<jats:sup>+<\/jats:sup>cells and p-Akt1<jats:sup>+<\/jats:sup>cells in the bone marrow. Deletion of Akt1 reduced Sca1<jats:sup>+<\/jats:sup>cells in the bone marrow and BAL. More importantly, 91.3\u2009\u00b1\u20094.9% bone marrow and 77.8\u2009\u00b1\u20094.9% lung \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>VE-cadherin<jats:sup>+<\/jats:sup>cells expressed Flk1, which is a key marker of endothelial progenitor cells (EPCs). Vagotomy reduced \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>VE-cadherin<jats:sup>+<\/jats:sup>p-Akt1<jats:sup>+<\/jats:sup>cells in the bone marrow and lung from pneumonia mice. Treatment with cultured EPCs reduced ELW compared to PBS treatment in<jats:italic>E. coli<\/jats:italic>pneumonia mice at 48\u2009h. The ELW was further reduced by treatment with EPCs combining with \u03b17nAChR agonist-PHA568487 compared to EPC treatments only.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Vagal \u03b17nAChR signaling regulates \u03b17nAChR<jats:sup>+<\/jats:sup>Sca1<jats:sup>+<\/jats:sup>VE-cadherin<jats:sup>+<\/jats:sup>EPCs via phosphorylation of Akt1 during lung injury repair in pneumonia.<\/jats:p><\/jats:sec>","DOI":"10.1186\/s13287-020-01892-4","type":"journal-article","created":{"date-parts":[[2020,8,31]],"date-time":"2020-08-31T10:03:10Z","timestamp":1598868190000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Vagal \u03b17nAChR signaling regulates \u03b17nAChR+Sca1+ cells during lung injury repair"],"prefix":"10.1186","volume":"11","author":[{"given":"Xiaoyan","family":"Chen","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jie","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yuanlin","family":"Song","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiao","family":"Su","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2020,8,31]]},"reference":[{"issue":"5","key":"1892_CR1","doi-asserted-by":"crossref","first-page":"L717","DOI":"10.1152\/ajplung.00132.2019","volume":"317","author":"JE Gotts","year":"2019","unstructured":"Gotts JE, Bernard O, Chun L, Croze RH, Ross JT, Nesseler N, et al. 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All experimental procedures were performed in accordance with the United States National Institutes of Health Guide for the Care and Use of Laboratory Animals (8th Edition, 2011).","order":1,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"The authors declare that they have no competing interests.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"375"}}