Article

Role of Staphylococcus aureus Catalase in Niche Competition against Streptococcus pneumoniae

Division of Pediatric Infectious Diseases and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.
Journal of bacteriology (Impact Factor: 2.81). 05/2008; 190(7):2275-8. DOI: 10.1128/JB.00006-08
Source: PubMed

ABSTRACT

Nasal colonization by Staphylococcus aureus is a major predisposing factor for subsequent infection. Recent reports of increased S. aureus colonization among children receiving pneumococcal vaccine implicate Streptococcus pneumoniae as an important competitor for the same niche. Since S. pneumoniae uses H2O2 to kill competing bacteria, we hypothesized that oxidant defense could play a significant role in promoting S. aureus colonization of the nasal mucosa. Using targeted mutagenesis, we showed that S. aureus expression of catalase contributes significantly to the survival of this pathogen in the presence of S. pneumoniae both in vitro and in a murine model of nasal cocolonization.

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    • "These enzymes are not only known to help bacterial cells compensate for various stress conditions but have also been suggested to have other physiological functions in S. aureus strains[26,27]. Other proteins that were up-regulated by kendomycin treatment included catalase (KatA), an enzyme that neutralizes H 2 O 2 under oxidative stress conditions[28], and succinate dehydrogenase flavoprotein subunit A (SdhA), a component of the only enzyme complex of the TCA cycle that can directly feed electrons into the respiratory chain[29]. The up-regulation of SdhA after kendomycin treatment most likely occurred to compensate for the breakdown of energy metabolism. "
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    • "Bacterial competition using inhibitory growth factors is not uncommon. For instance, in humans hydrogen peroxide produced by Streptococcus pneumoniae inhibits the growth of other respiratory tract microorganisms such as Haemophilus influenzae, Neisseria meningitidis, Moraxella catarrhalis and S. aureus (Park et al., 2008). Another possible explanation could be the local depletion of a vital factor necessary for growth after an intense proliferation of the experimental strain of S. aureus, favoring other microorganisms with different metabolic necessities to proliferate and replace the original strain. "
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    • "For bacterial enumeration, the mice were euthanized using isoflurane followed by cervical dislocation, and the nasal tissue was homogenized and vortexed for 5 min in PBS, and the homogenate was plated on THA with or without streptomycin after appropriate serial dilutions. Bacterial identification was based on antibiotic resistance patterns, colony morphology, and color as previously described [10]. Briefly, we have shown that mice (n = 5) administered PBS alone in the nose, harbor on average 1.9×106 CFU per nose, but none of the endogenous bacteria grew on streptomycin (500 µg/ml) plates (Figure S1). "
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