Current concepts in the role of the host response in Neisseria meningitidis septic shock

Curr Opin Infect Dis. 2002 Jun;15(3):247-52. doi: 10.1097/00001432-200206000-00006.

Abstract

Lipopolysaccharides in the outer membrane of Neisseria meningitidis are key molecules that induce inflammation and cause meningitis and shock. Mutant strains, with altered lipid A, the toxic moiety of lipopolysaccharide, or completely lacking lipopolysaccharide, induce significantly less inflammation than wild-type strains. Polymorphism of the Fc gamma receptors and interleukin-10 gene but not of the Toll-like receptor 4 may influence the development of meningococcal infection. Mannan-binding lectin is involved in complement activation, the regulation of adhesion molecules and cytokine production induced by meningococci. The activation of protein C by the thrombomodulin protein C receptor complex on the endothelial cell surface appears to be reduced in meningococcal sepsis but is still sufficient to convert protein C to activated protein C in patients treated with concentrated protein C.

Publication types

  • Review

MeSH terms

  • Carrier Proteins / immunology
  • Collectins
  • Drosophila Proteins*
  • Erythrocytes / cytology
  • Erythrocytes / metabolism
  • Erythrocytes / microbiology
  • Humans
  • Leukocytes / cytology
  • Leukocytes / metabolism
  • Leukocytes / microbiology
  • Lipopolysaccharides / chemistry
  • Lipopolysaccharides / immunology*
  • Lipopolysaccharides / toxicity
  • Membrane Glycoproteins / metabolism
  • Meningitis, Meningococcal / complications
  • Meningitis, Meningococcal / immunology*
  • Meningitis, Meningococcal / pathology
  • Meningitis, Meningococcal / physiopathology
  • Neisseria meningitidis / genetics
  • Neisseria meningitidis / immunology*
  • Neisseria meningitidis / metabolism
  • Protein C / metabolism
  • Receptors, Cell Surface / metabolism
  • Receptors, IgG / genetics
  • Receptors, IgG / metabolism
  • Shock, Septic / diagnosis
  • Shock, Septic / etiology
  • Shock, Septic / immunology*
  • Shock, Septic / physiopathology
  • Toll-Like Receptor 4
  • Toll-Like Receptors

Substances

  • Carrier Proteins
  • Collectins
  • Drosophila Proteins
  • Lipopolysaccharides
  • Membrane Glycoproteins
  • Protein C
  • Receptors, Cell Surface
  • Receptors, IgG
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Toll-Like Receptors