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Penicillin enhances the toll-like receptor 2-mediated proinflammatory activity of Streptococcus pneumoniae

Lisa J Moore1, Alison C Pridmore, Steven K Dower

  • 1Division of Genomic Medicine, University of Sheffield Medical School, Sheffield, United Kingdom.

The Journal of Infectious Diseases
|September 27, 2003
PubMed

Insights

Penicillin treatment releases inflammatory Streptococcus pneumoniae cell-wall components that activate Toll-like receptor 2 (TLR2). This activation depends on autolysin, bacterial growth phase, and antibiotic concentration.

Area of Science:

  • Microbiology
  • Immunology
  • Pharmacology

Background:

  • Streptococcus pneumoniae cell-wall components, peptidoglycan and lipoteichoic acid, activate Toll-like receptor 2 (TLR2).
  • TLR2 activation initiates inflammatory responses.
  • The impact of sub-inhibitory antibiotic concentrations on bacterial-induced immune activation is not fully understood.

Purpose of the Study:

  • To investigate how penicillin treatment affects TLR2 activation by S. pneumoniae.
  • To determine the role of bacterial autolysin in this process.
  • To examine the influence of bacterial growth phase and antibiotic concentration on TLR2 activation.

Main Methods:

  • Utilized TLR2-transfected HeLa cells to measure interleukin-8 promoter activity.
  • Exposed S. pneumoniae strain D39 and an autolysin-deficient mutant (AL2) to varying penicillin concentrations.
  • Assessed the effect of heat treatment and autolysin inhibitors on TLR2 activation.

Main Results:

  • Penicillin-treated S. pneumoniae D39 induced significantly enhanced IL-8 promoter activity compared to the autolysin-deficient mutant AL2.
  • TLR2 activation was enhanced by sub-MIC penicillin levels in lag-phase bacteria, while early log-phase bacteria responded most to MIC levels.
  • Heat treatment did not abolish enhancement, but autolysin inhibitors attenuated it.
  • Moxifloxacin and erythromycin did not show associated TLR2 activation.

Conclusions:

  • Penicillin treatment releases proinflammatory cell-wall components from S. pneumoniae that activate TLR2.
  • Autolysin activity is crucial for this penicillin-induced TLR2 activation.
  • Bacterial growth phase and antibiotic concentration modulate the extent of TLR2 activation.

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