{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T18:55:51Z","timestamp":1789757751401,"version":"4.0.1"},"reference-count":63,"publisher":"American Society for Microbiology","issue":"21","license":[{"start":{"date-parts":[[2016,11,1]],"date-time":"2016-11-01T00:00:00Z","timestamp":1477958400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000060","name":"HHS | NIH | National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R01 AI097157"],"award-info":[{"award-number":["R01 AI097157"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Bacteriol"],"published-print":{"date-parts":[[2016,11]]},"abstract":"ABSTRACT<\/jats:title>\n \n Neisseria gonorrhoeae<\/jats:named-content>\n (gonococci) and\n Neisseria meningitidis<\/jats:named-content>\n (meningococci) are human pathogens that cause gonorrhea and meningococcal meningitis, respectively. Both\n N. gonorrhoeae<\/jats:named-content>\n and\n N. meningitidis<\/jats:named-content>\n release a number of small peptidoglycan (PG) fragments, including proinflammatory PG monomers, although\n N. meningitidis<\/jats:named-content>\n releases fewer PG monomers. The PG fragments released by\n N. gonorrhoeae<\/jats:named-content>\n and\n N. meningitidis<\/jats:named-content>\n are generated in the periplasm during cell wall remodeling, and a majority of these fragments are transported into the cytoplasm by an inner membrane permease, AmpG; however, a portion of the PG fragments are released into the extracellular environment through unknown mechanisms. We previously reported that the expression of meningococcal\n ampG<\/jats:italic>\n in\n N. gonorrhoeae<\/jats:named-content>\n reduced PG monomer release by gonococci. This finding suggested that the efficiency of AmpG-mediated PG fragment recycling regulates the amount of PG fragments released into the extracellular milieu. We determined that three AmpG residues near the C-terminal end of the protein modulate AmpG's efficiency. We also investigated the association between PG fragment recycling and release in two species of human-associated nonpathogenic\n Neisseria<\/jats:named-content>\n :\n N. sicca<\/jats:named-content>\n and\n N. mucosa<\/jats:named-content>\n . Both\n N. sicca<\/jats:named-content>\n and\n N. mucosa<\/jats:named-content>\n release lower levels of PG fragments and are more efficient at recycling PG fragments than\n N. gonorrhoeae<\/jats:named-content>\n . Our results suggest that\n N. gonorrhoeae<\/jats:named-content>\n has evolved to increase the amounts of toxic PG fragments released by reducing its PG recycling efficiency.\n <\/jats:p>\n \n IMPORTANCE<\/jats:bold>\n Neisseria gonorrhoeae<\/jats:named-content>\n and\n Neisseria meningitidis<\/jats:named-content>\n are human pathogens that cause highly inflammatory diseases, although\n N. meningitidis<\/jats:named-content>\n is also frequently found as a normal member of the nasopharyngeal microbiota. Nonpathogenic\n Neisseria<\/jats:named-content>\n , such as\n N. sicca<\/jats:named-content>\n and\n N. mucosa<\/jats:named-content>\n , also colonize the nasopharynx without causing disease. Although all four species release peptidoglycan fragments,\n N. gonorrhoeae<\/jats:named-content>\n is the least efficient at recycling and releases the largest amount of proinflammatory peptidoglycan monomers, partly due to differences in the recycling permease AmpG. Studying the interplay between bacterial physiology (peptidoglycan metabolism) and pathogenesis (release of toxic monomers) leads to an increased understanding of how different bacterial species maintain asymptomatic colonization or cause disease and may contribute to efforts to mitigate disease.\n <\/jats:p>","DOI":"10.1128\/jb.00437-16","type":"journal-article","created":{"date-parts":[[2016,8,22]],"date-time":"2016-08-22T22:18:58Z","timestamp":1471904338000},"page":"3029-3040","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["Neisseria gonorrhoeae Crippled Its Peptidoglycan Fragment Permease To Facilitate Toxic Peptidoglycan Monomer Release"],"prefix":"10.1128","volume":"198","author":[{"given":"Jia Mun","family":"Chan","sequence":"first","affiliation":[{"name":"University of Wisconsin\u2014Madison, Department of Medical Microbiology and Immunology, School of Medicine and Public Health, Madison, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph P.","family":"Dillard","sequence":"additional","affiliation":[{"name":"University of Wisconsin\u2014Madison, Department of Medical Microbiology and Immunology, School of Medicine and Public Health, Madison, Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/JB.00542-10"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1186\/1471-2180-9-259"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1099\/mic.0.000086"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1136\/jcp.36.2.213"},{"key":"e_1_3_3_6_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0011835"},{"key":"e_1_3_3_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00506-12"},{"key":"e_1_3_3_8_2","first-page":"931","article-title":"Diagnosis and management of gonococcal infections","volume":"86","author":"Mayor MT","year":"2012","unstructured":"Mayor MT, Roett MA, Uduhiri KA. 2012. 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