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Polysaccharide intercellular adhesin.

Coagulase-negative staphylococci, with Staphylococcus epidermidis as the most frequently isolated species, have become the leading cause of hospital-acquired infections and infections of indwelling medical devices. In the course of these infections, biofilm formation and the ability to escape from host immune defense are regarded as the main virulence determinants. However, the factors protecting S. epidermidis from the immune system have remained elusive. Scientists have discovered the first specific molecule involved in immune evasion in S. epidermidis. The exopolysaccharide polysaccharide intercellular adhesin (PIA) was located at the cell surface of S. epidermidis; it protected organisms against phagocytosis by neutrophils, antibacterial peptides from human skin, and neutrophil granula. PIA was also indispensable for the formation of cellular aggregates. The positively charged PIA likely functions both as a mechanical barrier against peptides and phagocytes, and by electrostatic repulsion of the predominantly cationic antibacterial peptides. Thus, by inhibiting major mechanisms of the human innate immune defense, PIA may significantly contribute to the success of S. epidermidis in chronic infections. Interestingly, the genetic basis for PIA production is present in an increasing number of microorganisms, including such pathogenic species as Yersinia pestis, the causative agent of plague. Targeting PIA as a crucial component of both cell-cell aggregation and immune evasion processes might therefore constitute a promising way to interfere with the virulence of a series of important bacterial pathogens.

Vuong C, Voyich JM, Fischer ER, Braughton KR, Whitney AR, DeLeo FR, et al. Polysaccharide intercellular adhesion (PIA) protects Staphylococcus epidermidis against major components of the human innate immune system. Cell Microbiol. 2004;6:269-75.
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Title Annotation:Microbial Virulence
Author:McDade, Joseph E.
Publication:Emerging Infectious Diseases
Article Type:Brief Article
Date:Jun 1, 2004
Previous Article:Chagas disease.
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