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Bacterial hydrogen peroxide contributes to cerebral hyperemia during early stages of experimental pneumococcal

Olaf M Hoffmann1, Doreen Becker, Joerg R Weber

  • 1Department of Experimental Neurology, Center for Anatomy, Charité-Universitaetsmedizin Berlin, Berlin, Germany. joerg.weber@charite.de

Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism
|February 22, 2007
PubMed

Insights

Bacterial hydrogen peroxide (H2O2) from Streptococcus pneumoniae causes cerebral hyperperfusion in meningitis. This finding reveals bacterial H2O2 as a vasodilator, impacting blood flow during invasive infections.

Area of Science:

  • Neuroscience
  • Infectious Diseases
  • Microbiology

Background:

  • Alterations in blood flow are critical in invasive infections like sepsis and bacterial meningitis.
  • Streptococcus pneumoniae, a common cause of bacterial meningitis, uniquely produces hydrogen peroxide (H2O2) due to lacking functional catalase.

Purpose of the Study:

  • To investigate the impact of bacterial H2O2 production on regional cerebral blood flow (rCBF) and intracranial pressure (ICP) in experimental meningitis.

Main Methods:

  • A 6-hour rat model of experimental meningitis was used.
  • Regional cerebral blood flow (rCBF) and intracranial pressure (ICP) were measured.
  • Experiments involved wild-type D39 pneumococci, an H2O2-defective SpxB(-) mutant, and treatments with catalase and tetraethylammonium (TEA).

Main Results:

  • Meningitis induced by H2O2-defective pneumococci showed a significantly diminished rCBF increase compared to wild-type.
  • Treatment with catalase or TEA in wild-type induced meningitis also reduced rCBF increase.
  • Catalase treatment did not significantly affect the rCBF increase in the SpxB(-) mutant group.

Conclusions:

  • Bacterial-derived H2O2 acts as a potent vasodilator in pneumococcal meningitis.
  • Bacterial H2O2 contributes to early cerebral hyperperfusion, alongside host-mediated factors.
  • Understanding this mechanism is crucial for managing invasive infections caused by Streptococcus pneumoniae.

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