Group B streptococcal β-hemolysin induces nitric oxide production in murine macrophages

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

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35 Citations (Scopus)


Group B streptococcus (GBS) is the leading cause of sepsis in neonates. Nitric oxide (NO) release plays a role in the hypotension that characterizes septic shock. To examine the role of the GBS β-hemolysin in NO production, the murine macrophage line RAW 264.7 was exposed to a wild-type (WT) GBS isolate and to hyperhemolytic (HH) and nonhemolytic (NH) transposon mutants derived from that isolate. After activation of macrophages by the WT strain, the HH mutant, or cell-free extracts of β-hemolysin, nitrite release into the supernatanr increased >10-fold and inducible NO synthase (iNOS) levels in cell lysates increased up to 10-fold compared with treatment with the NH mutant or extracts from that mutant. Hemolysin-induced NO production was dependent on protein tyrosine kinases and NF-κB, but not on extracellular signal-related kinase-1/2-mitogen-activated kinases or protein kinase A. These results indicate that GBS β-hemolysin induces murine macrophage iNOS via intracellular pathways similar to those that mediate lipopolysaccharide- induced iNOS activation.

Original languageEnglish
Pages (from-to)150-157
Number of pages8
JournalJournal of Infectious Diseases
Issue number1
Publication statusPublished - 2000
Externally publishedYes

ASJC Scopus subject areas

  • General Medicine


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