Open AccessPolysaccharide intercellular adhesin (PIA) protects Staphylococcus epidermidis against major components of the human innate immune system
Author(s) -
Vuong Cuong,
Voyich Jovanka M.,
Fischer Elizabeth R.,
Braughton Kevin R.,
Whitney Adeline R.,
DeLeo Frank R.,
Otto Michael
Publication year - 2004
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1046/j.1462-5822.2004.00367.x
Subject(s) - innate immune system , microbiology and biotechnology , biology , staphylococcus epidermidis , bacterial adhesin , biofilm , immune system , phagocytosis , pathogen , human pathogen , staphylococcus aureus , immunology , bacteria , virulence , biochemistry , genetics , gene
Summary The skin commensal and opportunistic pathogen Staphylococcus epidermidis is the leading cause of nosocomial and biofilm‐associated infections. Little is known about the mechanisms by which S. epidermidis protects itself against the innate human immune system during colonization and infection. We used scanning electron microscopy to demonstrate that the exopolysaccharide intercellular adhesin (PIA) resides in fibrous strands on the bacterial cell surface, and that lack of PIA production results in complete loss of the extracellular matrix material that has been suggested to mediate immune evasion. Phagocytosis and killing by human polymorphonuclear leucocytes was significantly increased in a mutant strain lacking PIA production compared with the wild‐type strain. The mutant strain was also significantly more susceptible to killing by major antibacterial peptides of human skin, cationic human β‐defensin 3 and LL‐37, and anionic dermcidin. PIA represents the first defined factor of the staphylococcal biofilm matrix that protects against major components of human innate host defence.