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The biologic activities of peptidoglycan in experimental Haemophilus influenzae meningitis

M Burroughs1, S Prasad, C Cabellos

  • 1Laboratory of Molecular Infectious Diseases, Rockefeller University, New York, NY 10021.

The Journal of Infectious Diseases
|February 1, 1993
PubMed

Insights

Gram-negative peptidoglycan from Haemophilus influenzae causes brain edema in meningitis. This component is more potent than the intact cell wall and contributes significantly to disease pathology.

Area of Science:

  • Microbiology
  • Immunology
  • Pathology

Background:

  • Gram-positive bacterial cell walls are known inflammatory agents.
  • The role of gram-negative peptidoglycan in disease pathogenesis remains largely uncharacterized.

Purpose of the Study:

  • To investigate the inflammatory potential of Haemophilus influenzae peptidoglycan in a rabbit meningitis model.
  • To compare the bioactivity of intact cell wall, purified peptidoglycan, and soluble subcomponents.

Main Methods:

  • Administration of Haemophilus influenzae cell wall, purified peptidoglycan, and subcomponents into rabbit cerebrospinal fluid (CSF).
  • Assessment of brain edema, CSF leukocytosis, and protein accumulation.
  • Evaluation of peptidoglycan from ampicillin-resistant versus sensitive strains.
  • Analysis of ampicillin-induced bacterial lysates with neutralized endotoxin.

Main Results:

  • Haemophilus peptidoglycan induced brain edema at concentrations as low as 0.1 µg/mL in CSF.
  • Leukocytosis and protein accumulation in CSF required higher concentrations (≥10.0 µg/mL).
  • Solubilized peptidoglycan was 10-fold more potent than intact cell wall; resistant strains showed twofold greater bioactivity.

Conclusions:

  • Peptidoglycan from gram-negative bacteria, specifically Haemophilus influenzae, contributes to the pathology of meningitis.
  • Peptidoglycan is a significant driver of brain edema in this condition.
  • The inflammatory effects are more pronounced with solubilized peptidoglycan and from antibiotic-resistant strains.

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