{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T21:24:06Z","timestamp":1792185846234,"version":"4.4.0"},"reference-count":35,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2014,1,1]],"date-time":"2014-01-01T00:00:00Z","timestamp":1388534400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2014,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            <jats:named-content content-type=\"genus-species\">Neisseria gonorrhoeae<\/jats:named-content>\n            causes gonorrhea, a sexually transmitted infection characterized by inflammation of the cervix or urethra. However, a significant subset of patients with\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            remain asymptomatic, without evidence of localized inflammation. Inflammatory responses to\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            are generated by host innate immune recognition of\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            by several innate immune signaling pathways, including lipooligosaccharide (LOS) and other pathogen-derived molecules through activation of innate immune signaling systems, including toll-like receptor 4 (TLR4) and the interleukin-1\u03b2 (IL-1\u03b2) processing complex known as the inflammasome. The lipooligosaccharide of\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            has a hexa-acylated lipid A.\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            strains that carry an inactivated\n            <jats:italic>msbB<\/jats:italic>\n            (also known as\n            <jats:italic>lpxL1<\/jats:italic>\n            ) gene produce a penta-acylated lipid A and exhibit reduced biofilm formation, survival in epithelial cells, and induction of epithelial cell inflammatory signaling. We now show that\n            <jats:italic>msbB<\/jats:italic>\n            -deficient\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            induces less inflammatory signaling in human monocytic cell lines and murine macrophages than the parent organism. The penta-acylated LOS exhibits reduced toll-like receptor 4 signaling but does not affect\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            -mediated activation of the inflammasome. We demonstrate that\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            <jats:italic>msbB<\/jats:italic>\n            is dispensable for initiating and maintaining infection in a murine model of gonorrhea. Interestingly, infection with\n            <jats:italic>msbB<\/jats:italic>\n            -deficient\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            is associated with less localized inflammation. Combined, these data suggest that TLR4-mediated recognition of\n            <jats:named-content content-type=\"genus-species\">N. gonorrhoeae<\/jats:named-content>\n            LOS plays an important role in the pathogenesis of symptomatic gonorrhea infection and that alterations in lipid A biosynthesis may play a role in determining symptomatic and asymptomatic infections.\n          <\/jats:p>","DOI":"10.1128\/iai.00890-13","type":"journal-article","created":{"date-parts":[[2013,10,15]],"date-time":"2013-10-15T00:16:11Z","timestamp":1381796171000},"page":"184-192","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":26,"title":["Hexa-Acylated Lipid A Is Required for Host Inflammatory Response to Neisseria gonorrhoeae in Experimental Gonorrhea"],"prefix":"10.1128","volume":"82","author":[{"given":"Xiyou","family":"Zhou","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi","family":"Gao","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter M.","family":"Broglie","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chahnaz","family":"Kebaier","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James E.","family":"Anderson","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natalie","family":"Thom","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases, University of North Carolina, Chapel Hill, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael A.","family":"Apicella","sequence":"additional","affiliation":[{"name":"Departments of Microbiology and Internal Medicine, The Carver College of Medicine, The University of Iowa, Iowa City, Iowa, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gregory D.","family":"Sempowski","sequence":"additional","affiliation":[{"name":"Departments of Medicine, Pathology, and the Duke Human Vaccine Institute, Duke University Medical Center, Durham, North Carolina, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph 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