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Therefore, we create <jats:italic>Mptx2<\/jats:italic> knockout (<jats:italic>Mptx2<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>) mice to investigate its precise effects on intestinal homeostasis using models of lipopolysaccharide (LPS), methicillin-resistant <jats:italic>Staphylococcus aureus<\/jats:italic> (<jats:italic>MRSA<\/jats:italic>) peritoneal infection, and dextran sulfate sodium (DSS)\u2013induced intestinal injury and inflammation. We here find that <jats:italic>Mptx2<\/jats:italic> is selectively expressed in Paneth cells in the small intestines of mice. <jats:italic>Mptx2<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice have increased susceptibility to intestinal inflammation and injured. Mptx2 deficiency reduces Paneth cell count and expression of antimicrobial factors, leading to altered intestinal bacteria composition. Loss of <jats:italic>Mptx2<\/jats:italic> aggravates MRSA infection\u2013induced damage in the intestine while decreasing autophagy in Paneth cells. <jats:italic>Mptx2<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice are more vulnerable to LPS-induced intestinal possibly due to inhibition of the autophagy\/endoplasmic reticulum (ER) stress pathway. <jats:italic>Mptx2<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup> mice are susceptible to DSS-induced colitis that could be ameliorated by treatment with gentamicin or vancomycin antibiotics. In conclusion, Mptx2 is essential to maintain intestinal homeostasis potentially via regulation of autophagy in Paneth cells.<\/jats:p>","DOI":"10.1038\/s42003-024-05785-7","type":"journal-article","created":{"date-parts":[[2024,1,13]],"date-time":"2024-01-13T10:02:19Z","timestamp":1705140139000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Loss of Mptx2 alters bacteria composition and intestinal homeostasis potentially by impairing autophagy"],"prefix":"10.1038","volume":"7","author":[{"given":"Weihui","family":"Yan","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shanshan","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaying","family":"You","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ying","family":"Lu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weipeng","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bo","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Du","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shicheng","family":"Peng","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4355-5693","authenticated-orcid":false,"given":"Wei","family":"Cai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0964-609X","authenticated-orcid":false,"given":"Yongtao","family":"Xiao","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,1,13]]},"reference":[{"key":"5785_CR1","doi-asserted-by":"publisher","first-page":"275","DOI":"10.1007\/s12263-007-0058-x","volume":"2","author":"C van der Meer-van Kraaij","year":"2007","unstructured":"van der Meer-van Kraaij, C. et al. 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