{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T14:08:06Z","timestamp":1790518086033,"version":"4.1.0"},"reference-count":49,"publisher":"American Society for Microbiology","issue":"1","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"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":[[2013,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Loss of phosphoethanolamine (PEA) from the lipid A of gonococcal strain FA19 results in increased sensitivity to killing by the classical pathway of complement. Here we demonstrate that loss of PEA from lipid A diminishes binding of the complement regulatory protein C4b binding protein (C4BP) to the FA19 porin B (PorB), providing a molecular basis to explain the susceptibility of an<jats:italic>lptA<\/jats:italic>null strain of FA19 to killing by normal human serum (NHS). Loss of PEA from lipid A in three additional gonococcal strains that expressed diverse PorB molecules also resulted in decreased C4BP binding, increased deposition of C4b, and increased susceptibility to killing by NHS. Complementation of<jats:italic>lptA<\/jats:italic>null strains with<jats:italic>lptA<\/jats:italic>restored C4BP binding, decreased C4b deposition, and increased resistance to killing by NHS. These effects of lipid A PEA on C4BP binding to gonococcal PorB and serum resistance were simulated when gonococcal PorB was expressed in a meningococcal background. Loss of PEA from lipid A also affected binding of the alternative pathway regulator factor H (fH) to PorB of some strains. For instance, PorB molecules of<jats:italic>lptA<\/jats:italic>null mutants of strains 252 and 1291 bound less fH than those of their parent strains when lipooligosaccharide (LOS) was sialylated, whereas PorB molecules of<jats:italic>lptA<\/jats:italic>null mutants of strains FA1090 and 273 retained the ability to bind fH when LOS was sialylated. These data indicate that replacement of lipid A with PEA alters binding of C4BP and fH to PorB and contributes to the ability of gonococci to resist complement-mediated killing.<\/jats:p>","DOI":"10.1128\/iai.00751-12","type":"journal-article","created":{"date-parts":[[2012,10,16]],"date-time":"2012-10-16T01:48:39Z","timestamp":1350352119000},"page":"33-42","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":43,"title":["Phosphoethanolamine Residues on the Lipid A Moiety of Neisseria gonorrhoeae Lipooligosaccharide Modulate Binding of Complement Inhibitors and Resistance to Complement Killing"],"prefix":"10.1128","volume":"81","author":[{"given":"Lisa A.","family":"Lewis","sequence":"first","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts School of Medicine, Worcester, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William M.","family":"Shafer","sequence":"additional","affiliation":[{"name":"Laboratories of Bacterial Pathogenesis, Medical Research Service, Veterans Affairs Medical Center (Atlanta), Decatur, Georgia, USA"},{"name":"Department of Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tathagat","family":"Dutta Ray","sequence":"additional","affiliation":[{"name":"Department of Medicine, New York University School of Medicine, New York, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay","family":"Ram","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts School of Medicine, Worcester, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter A.","family":"Rice","sequence":"additional","affiliation":[{"name":"Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts School of Medicine, Worcester, Massachusetts, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","unstructured":"World Health Organization (WHO) Department of Reproductive Health and Research. 2012. 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