Inhibition of nitric oxide synthase exacerbates group B streptococcus sepsis and arthritis in mice

Infect Immun. 2004 Aug;72(8):4891-4. doi: 10.1128/IAI.72.8.4891-4894.2004.

Abstract

The role of nitric oxide in group B Streptococcus (GBS) infection was evaluated by inhibiting its production with aminoguanidine (AG). AG-treated mice displayed higher mortality rates and more frequent and severe arthritis than controls. Worsening of arthritis correlated with a higher number of GBS cells in the joints and local interleukin-1 beta production.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Outbred Strains
  • Arthritis, Infectious / drug therapy
  • Arthritis, Infectious / microbiology
  • Arthritis, Infectious / mortality
  • Arthritis, Infectious / physiopathology*
  • Enzyme Inhibitors / administration & dosage
  • Enzyme Inhibitors / pharmacology*
  • Female
  • Guanidines / administration & dosage
  • Guanidines / pharmacology*
  • Humans
  • Male
  • Mice
  • Nitric Oxide / physiology*
  • Nitric Oxide / urine
  • Nitric Oxide Synthase / antagonists & inhibitors*
  • Nitric Oxide Synthase Type II
  • Sepsis / drug therapy
  • Sepsis / mortality
  • Sepsis / physiopathology*
  • Severity of Illness Index
  • Streptococcal Infections / drug therapy
  • Streptococcal Infections / microbiology
  • Streptococcal Infections / mortality
  • Streptococcal Infections / physiopathology*
  • Streptococcus agalactiae / pathogenicity*

Substances

  • Enzyme Inhibitors
  • Guanidines
  • Nitric Oxide
  • NOS2 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type II
  • Nos2 protein, mouse
  • pimagedine