Abstract
Background Pathogenic bacteria incessantly evolve mechanisms to resist their host’s innate immunity. One such mechanism is molecular camouflage: the modification of bacterial surface molecules to make them unrecognizable by the host’s immune system or resistant to its effector molecules. Recently, a peptidoglycan deacetylase (PgdA) was discovered in Streptococcus pneumoniae that renders bacterial peptidoglycan resistant to human lysozyme, thus preventing host-mediated cell wall damage [1-3]. In addition, polysaccharide deacetylases with different substrate specificities were identified in other
Highlights
Pathogenic bacteria incessantly evolve mechanisms to resist their host’s innate immunity
Materials and methods In this study, genomes of streptococci and other representative gram-positive cocci were screened for the presence of functional homologs of PgdA, the prototypic pneumococcal peptidoglycan deacetylase
The ConSurf tool[7,8] was used for surface mapping of the phylogenetic information calculated from the multiple sequence alignments
Summary
Pathogenic bacteria incessantly evolve mechanisms to resist their host’s innate immunity. One such mechanism is molecular camouflage: the modification of bacterial surface molecules to make them unrecognizable by the host’s immune system or resistant to its effector molecules. A peptidoglycan deacetylase (PgdA) was discovered in Streptococcus pneumoniae that renders bacterial peptidoglycan resistant to human lysozyme, preventing host-mediated cell wall damage [1,2,3]. Polysaccharide deacetylases with different substrate specificities were identified in other. Gram-positive bacteria and shown to contribute to virulence (e.g., IcaB of Staphylococcus epidermidis [4] and Pdi or Streptococcus iniae [5])
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