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Staphylococcus epidermidis  and  Staphylococcus aureus  are leading causes of hospital-acquired infections that have become increasingly difficult to treat due to the prevalence of antibiotic resistance in these organisms. The ability of staphylococci to produce biofilm is an important virulence mechanism that allows bacteria both to adhere to living and artificial surfaces and to resist host immune factors and antibiotics. Here, we show that the  icaADBC  locus, which synthesizes the biofilm-associated polysaccharide intercellular adhesin (PIA) in staphylococci, is required for the formation of a lethal  S. epidermidis  infection in the intestine of the model nematode  Caenorhabditis elegans . Susceptibility to  S. epidermidis  infection is influenced by mutation of the  C. elegans  PMK-1 p38 mitogen-activated protein (MAP) kinase or DAF-2 insulin-signaling pathways. Loss of PIA production abrogates nematocidal activity and leads to reduced bacterial accumulation in the  C. elegans  intestine, while overexpression of the  icaADBC  locus in  S. aureus  augments virulence towards nematodes. PIA-producing  S. epidermidis  has a significant survival advantage over  ica -deficient  S. epidermidis  within the intestinal tract of wild-type  C. elegans,  but not in immunocompromised nematodes harboring a loss-of-function mutation in the p38 MAP kinase pathway gene  sek-1 . Moreover,  sek-1  and  pmk-1  mutants are equally sensitive to wild-type and  icaADBC -deficient  S. epidermidis . These results suggest that biofilm exopolysaccharide enhances virulence by playing an immunoprotective role during colonization of the  C. elegans  intestine. These studies demonstrate that  C. elegans  can serve as a simple animal model for studying host–pathogen interactions involving staphylococcal biofilm exopolysaccharide and suggest that the protective activity of biofilm matrix represents an ancient conserved function for resisting predation.

Staphylococcal Biofilm Exopolysaccharide Protects against Caenorhabditis elegans Immune Defenses