Identification of Genes Particularly Sensitive to Lipopolysaccharide (LPS) in Human Monocytes Induced by Wild-Type versus LPS-DeficientNeisseria meningitidisStrains

Candidate inhibitors of porcine complement

“…It is for instance shown that LPS-deficient N. meningitides (LPS -) can activate the complement system and induce complement mediated inflammatory effects (148). N. meningitides (LPS -) have also been shown to be able to induce large gene expression changes in human monocytes (149). In study II, we found that anti-CD14 inhibited production of LPSinduced IL-8 production in whole blood, but not whole live E. coli-induced IL-8.…”

Global Effect of Interleukin-10 on the Transcriptional Profile Induced by Neisseria meningitidis in Human Monocytes

“…N. meningitidis strain 44/76 (serogroup B) was isolated from a culture of blood from a Norwegian patient with lethal meningococcal infection. The bacteria were serologically characterized, cultured, harvested, and heat inactivated at the Norwegian Institute of Public Health as previously described (43).…”

“…Human monocytes are highly responsive to meningococci. N. meningitidis and purified LPS from N. meningitidis induce an altered expression of more than 4,600 genes (43). Still, in vitro studies combining plasma from patients with fulminant septicemia with normal human donor monocytes suggest that the monocytes may not be activated in a shock plasma sample despite concurrent high levels of bioactive LPS (7).…”

Post-genomics ofNeisseria meningitidis: an update

“…Alterations of gene-expression profiles, mediated by lipopolysaccharide (LPS), were also investigated in human monocytes [28]. To address this, an LPS-deficient mutant of the MenB reference strain H44/76 was developed.…”

“…Between 2005 and 2008, many studies employed transcriptome analysis for the characterization of diverse aspects of N. meningitidis physiology, in particular regulation by the two-component signal transduction NMB0595/NMB0594 [22,23] and iron availability [24,25], as well as the host cell response to a live bacterial infection [26][27][28][29][30].…”