{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,4]],"date-time":"2026-03-04T12:53:38Z","timestamp":1772628818946,"version":"3.50.1"},"reference-count":50,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2010,12,1]],"date-time":"2010-12-01T00:00:00Z","timestamp":1291161600000},"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":[[2010,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The human airway epithelium is constantly exposed to microbial products from colonizing organisms. Regulation of Toll-like receptor (TLR) expression and specific interactions with bacterial ligands is thought to mitigate exacerbation of inflammatory processes induced by the commensal flora in these cells. The genus\n            <jats:italic>Neisseria<\/jats:italic>\n            comprises pathogenic and commensal organisms that colonize the human nasopharynx.\n            <jats:italic>Neisseria lactamica<\/jats:italic>\n            is not associated with disease, but\n            <jats:italic>N. meningitidis<\/jats:italic>\n            occasionally invades the host, causing meningococcal disease and septicemia. Upon colonization of the airway epithelium, specific host cell receptors interact with numerous\n            <jats:italic>Neisseria<\/jats:italic>\n            components, including the PorB porin, at the immediate bacterial-host cell interface. This major outer membrane protein is expressed by all\n            <jats:italic>Neisseria<\/jats:italic>\n            strains, regardless of pathogenicity, but its amino acid sequence varies among strains, particularly in the surface-exposed regions. The interaction of\n            <jats:italic>Neisseria<\/jats:italic>\n            PorB with TLR2 is essential for driving TLR2\/TLR1-dependent cellular responses and is thought to occur via the porin's surface-exposed loop regions. Our studies show that\n            <jats:italic>N. lactamica<\/jats:italic>\n            PorB is a TLR2 ligand but its binding specificity for TLR2 is different from that of meningococcal PorB. Furthermore,\n            <jats:italic>N. lactamica<\/jats:italic>\n            PorB is a poor inducer of proinflammatory mediators and of TLR2 expression in human airway epithelial cells. These effects are reproduced by whole\n            <jats:italic>N. lactamica<\/jats:italic>\n            organisms. Since the responsiveness of human airway epithelial cells to colonizing bacteria is in part regulated via TLR2 expression and signaling, commensal organisms such as\n            <jats:italic>N. lactamica<\/jats:italic>\n            would benefit from expressing a product that induces low TLR2-dependent local inflammation, likely delaying or avoiding clearance by the host.\n          <\/jats:p>","DOI":"10.1128\/iai.00681-10","type":"journal-article","created":{"date-parts":[[2010,10,12]],"date-time":"2010-10-12T04:59:31Z","timestamp":1286859571000},"page":"5314-5323","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":29,"title":["Human Airway Epithelial Cell Responses to\n            <i>Neisseria lactamica<\/i>\n            and Purified Porin via Toll-Like Receptor 2-Dependent Signaling"],"prefix":"10.1128","volume":"78","author":[{"given":"Xiuping","family":"Liu","sequence":"first","affiliation":[{"name":"Section of Infectious Diseases, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lee M.","family":"Wetzler","sequence":"additional","affiliation":[{"name":"Section of Infectious Diseases, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Laura","family":"Oliveira Nascimento","sequence":"additional","affiliation":[{"name":"School of Pharmaceutical Sciences, University of Sa\u0303o Paulo, Sa\u0303o Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Paola","family":"Massari","sequence":"additional","affiliation":[{"name":"Section of Infectious Diseases, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1074\/jbc.M110333200"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.cellsig.2008.12.001"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.170.12.6141"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2958.2004.04423.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.164.2.966"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0950268800066449"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1093\/clinids\/13.2.216"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.67.5.2406-2413.1999"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1034\/j.1600-065X.2000.917304.x"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00968-08"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.00644-06"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/137.2.112"},{"key":"e_1_3_2_14_2","first-page":"418","volume":"53","year":"2005","unstructured":"Greene, C. 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