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The genus\n              <jats:italic>Neisseria<\/jats:italic>\n              is also home to multiple species of human- or animal-associated\n              <jats:italic>Neisseria<\/jats:italic>\n              that form part of the normal microbiota. Here we characterized PG release from the human-associated nonpathogenic species\n              <jats:italic>Neisseria lactamica<\/jats:italic>\n              and\n              <jats:italic>Neisseria mucosa<\/jats:italic>\n              and animal-associated\n              <jats:italic>Neisseria<\/jats:italic>\n              from macaques and wild mice. An\n              <jats:italic>N. mucosa<\/jats:italic>\n              strain and an\n              <jats:italic>N. lactamica<\/jats:italic>\n              strain were found to release limited amounts of the proinflammatory monomeric PG fragments. However, a single amino acid difference in the PG fragment permease AmpG resulted in increased PG fragment release in a second\n              <jats:italic>N. lactamica<\/jats:italic>\n              strain examined.\n              <jats:italic>Neisseria<\/jats:italic>\n              isolated from macaques also showed substantial release of PG monomers. The mouse colonizer\n              <jats:italic>Neisseria musculi<\/jats:italic>\n              exhibited PG fragment release similar to that seen in\n              <jats:italic>N. gonorrhoeae<\/jats:italic>\n              with PG monomers being the predominant fragments released. All the human-associated species were able to stimulate NOD1 and NOD2 responses.\n              <jats:italic>N. musculi<\/jats:italic>\n              was a poor inducer of mouse NOD1, but\n              <jats:italic>ldcA<\/jats:italic>\n              mutation increased this response. The ability to genetically manipulate\n              <jats:italic>N. musculi<\/jats:italic>\n              and examine effects of different PG fragments or differing amounts of PG fragments during mouse colonization will lead to a better understanding of the roles of PG in\n              <jats:italic>Neisseria<\/jats:italic>\n              infections. Overall, we found that only some nonpathogenic\n              <jats:italic>Neisseria<\/jats:italic>\n              have diminished release of proinflammatory PG fragments, and there are differences even within a species as to types and amounts of PG fragments released.\n            <\/jats:p>\n          <\/jats:sec>","DOI":"10.1128\/iai.00004-24","type":"journal-article","created":{"date-parts":[[2024,4,2]],"date-time":"2024-04-02T14:17:17Z","timestamp":1712067437000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":6,"title":["Peptidoglycan fragment release and NOD activation by commensal\n            <i>Neisseria<\/i>\n            species from humans and other animals"],"prefix":"10.1128","volume":"92","author":[{"given":"Tiffany N.","family":"Harris-Jones","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jia Mun","family":"Chan","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathleen T.","family":"Hackett","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6597-4581","authenticated-orcid":true,"given":"Nathan J.","family":"Weyand","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Ohio University, Athens, Ohio, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5300-2403","authenticated-orcid":true,"given":"Ryan 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