{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T04:50:59Z","timestamp":1790225459127,"version":"4.1.0"},"reference-count":55,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2008,6,1]],"date-time":"2008-06-01T00:00:00Z","timestamp":1212278400000},"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":[[2008,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Lipopolysaccharide (LPS) in the outer membrane of<jats:italic>Neisseria meningitidis<\/jats:italic>plays a dominant role as an inflammation-inducing molecule in meningococcal disease. We have used microarray analysis to study the global gene expression after exposure of human monocytes for 3 h to wild-type<jats:italic>N. meningitidis<\/jats:italic>(10<jats:sup>6<\/jats:sup>), LPS-deficient<jats:italic>N. meningitidis<\/jats:italic>(10<jats:sup>6<\/jats:sup>and 10<jats:sup>8<\/jats:sup>), and purified<jats:italic>N. meningitidis<\/jats:italic>LPS (1 ng [33 endotoxin units]\/ml) to identify LPS-inducible genes. Wild-type<jats:italic>N. meningitidis<\/jats:italic>(10<jats:sup>6<\/jats:sup>) induced 4,689 differentially expressed genes, compared with 72 differentially expressed genes induced by 10<jats:sup>6<\/jats:sup>LPS-deficient<jats:italic>N. meningitidis<\/jats:italic>organisms. However, 10<jats:sup>8<\/jats:sup>LPS-deficient<jats:italic>N. meningitidis<\/jats:italic>organisms induced 3,905 genes, indicating a dose-response behavior of non-LPS cell wall molecules. A comparison of the gene expression patterns from 10<jats:sup>6<\/jats:sup>wild-type<jats:italic>N. meningitidis<\/jats:italic>and 10<jats:sup>8<\/jats:sup>LPS-deficient<jats:italic>N. meningitidis<\/jats:italic>organisms showed that 2,401 genes in human monocytes were not strictly LPS dependent. A list of \u201cparticularly LPS-sensitive\u201d genes (2,288), differentially induced by 10<jats:sup>6<\/jats:sup>wild-type<jats:italic>N. meningitidis<\/jats:italic>but not by 10<jats:sup>8<\/jats:sup>LPS-deficient<jats:italic>N. meningitidis<\/jats:italic>organisms, showed an early expression of beta interferon (IFN-\u03b2), most likely through the Toll-like receptor-MyD88-independent pathway. Subsequently, IFN-\u03b2 may activate the type I IFN signaling pathway, and an unknown number of IFN-\u03b2-inducible genes, such as those for CXCL9, CXCL10, CXCL11, IFIT1, IFIT2, IFIT3, and IFIT5, are transcribed. Supporting this, human monocytes secreted significantly higher levels of CXCL10 and CXCL11 when stimulated by 10<jats:sup>6<\/jats:sup>wild-type<jats:italic>N. meningitidis<\/jats:italic>organisms than when stimulated by 10<jats:sup>8<\/jats:sup>LPS-deficient<jats:italic>N. meningitidis<\/jats:italic>organisms. Plasma CXCL10, but not CXCL11, was positively correlated (<jats:italic>r<\/jats:italic>= 0.67;<jats:italic>P<\/jats:italic>&lt; 0.01) to LPS in patients (<jats:italic>n<\/jats:italic>= 24) with systemic meningococcal disease. Thus, new circulating biomarkers in meningococcal disease may be suggested through LPS-induced gene expression changes in human monocytes.<\/jats:p>","DOI":"10.1128\/iai.01625-07","type":"journal-article","created":{"date-parts":[[2008,3,25]],"date-time":"2008-03-25T00:24:38Z","timestamp":1206404678000},"page":"2685-2695","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":44,"title":["Identification of Genes Particularly Sensitive to Lipopolysaccharide (LPS) in Human Monocytes Induced by Wild-Type versus LPS-Deficient<i>Neisseria meningitidis<\/i>Strains"],"prefix":"10.1128","volume":"76","author":[{"given":"Reidun","family":"\u00d8vsteb\u00f8","sequence":"first","affiliation":[{"name":"Departments of Clinical Chemistry"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ole Kristoffer","family":"Olstad","sequence":"additional","affiliation":[{"name":"Departments of Clinical Chemistry"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Berit","family":"Brusletto","sequence":"additional","affiliation":[{"name":"Departments of Clinical Chemistry"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anne Sophie","family":"M\u00f8ller","sequence":"additional","affiliation":[{"name":"Departments of Clinical Chemistry"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Audun","family":"Aase","sequence":"additional","affiliation":[{"name":"Departments of Bacteriology and Immunology, The Norwegian Institute of Public Health"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kari Bente Foss","family":"Haug","sequence":"additional","affiliation":[{"name":"Departments of Clinical Chemistry"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Petter","family":"Brandtzaeg","sequence":"additional","affiliation":[{"name":"Pediatrics, Ulleval University Hospital"},{"name":"Faculty of Medicine, University of Oslo, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Kierulf","sequence":"additional","affiliation":[{"name":"Departments of Clinical Chemistry"},{"name":"Faculty of Medicine, University of Oslo, Oslo, Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0264-410X(02)00774-0"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1177\/09680519030090030301"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1177\/09680519000060060501"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/0003-2697(76)90527-3"},{"key":"e_1_3_2_6_2","first-page":"427","year":"2001","unstructured":"Brandtzaeg, P., R. \u00d8vsteb\u00f8, and P. 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