Group B streptococcal β-hemolysin induces mortality and liver injury in experimental sepsis

Axel Ring, Johann S. Braun, Jürgen Pohl, Victor Nizet, Wolfgang Stremmel, Jerry L. Shenep

Research output: Contribution to journalArticlepeer-review

45 Citations (Scopus)

Abstract

New Zealand White rabbits were challenged with the wild-type (wt) group B streptococci (GBS) serotype III strain (COH1) and its isogenic nonhemolytic (NH) and hyperhemolytic (HH) mutants. Mortality differed significantly between rabbits infected with the HH mutant IN40 (67%), compared with rabbits infected with the wt COH1 strain (27%) and the NH strains COH1-20 and COHl:cylEΔcat (13% and 0%, respectively; P < .05). Histopathologically, disseminated septic microabscesses surrounded by necrotic foci were found exclusively in the livers of HH mutant IN40-infected animals. Serum transaminase levels were 20-fold higher in the HH-infected group, compared with rabbits infected with the other strains. Positive TUNEL (in situ terminal deoxynucleotide transferase-mediated dUTP nick end labeling) staining and activation of caspase-3 in hepatocytes were more frequent in HH-infected than in wt-infected animals and absent in the NH mutant COH1-20-infected group, indicating that GBS β-hemolysin triggers apoptotic pathways in hepatocytes. This work provides the first evidence that GBS β-hemolysin plays a crucial role in the pathophysiology of GBS sepsis by inducing liver failure and high mortality.

Original languageEnglish
Pages (from-to)1745-1753
Number of pages9
JournalJournal of Infectious Diseases
Volume185
Issue number12
DOIs
Publication statusPublished - Jun 15 2002
Externally publishedYes

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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