Abstract
Host inflammatory response to meningococcal infection is believed to be a major determinant of disease severity. Isogenic mutants of Neisseria meningitidis serogroup B1940, which differ in expression of capsular polysaccharide and lipooligosaccharide (LOS), were used to examine host responses in a whole blood model of bacteremia and a model of endothelial injury. The parent organism caused significantly less neutrophil shedding of the adhesion molecule, L-selectin, than the three mutant organisms (P < .01) and was most resistant to the bactericidal activity of whole blood. Despite marked differences in bacterial adhesion to endothelial cells (P < .05), no damage was induced by organisms alone. Endothelial injury was observed when neutrophils were incubated with adherent, capsule-deficient organisms (P < .05). The degree of endothelial damage was related to the number of neutrophils adherent to the endothelium. Thus, bacterial capsulation and LOS structure can influence neutrophil activation and endothelial injury and, as such, may be important in the pathogenesis of meningococcal sepsis.
| Original language | English |
|---|---|
| Pages (from-to) | 172-179 |
| Number of pages | 8 |
| Journal | Journal of Infectious Diseases |
| Volume | 173 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1996 |
Bibliographical note
Funding Information:Received 17 February 1995; revised 10 July 1995. Grant support: Wellcome Advanced Training Fellowship (R.S.H.), Meningitis Research Appeal, Child Health Research Action Trust, and Deutsche Forschungsgemeinschaft (grant Fr689/8-1) and a professorship from the Hermann and Lilly Schilling Foundation (M.F.). Reprints or correspondence: N. J. Klein, Imrnunobiology Unit, Institute of Child Health, 30 Guilford St., London WCIN IEH, UK.
