Background: A major complication of using medical devices is the development of biofilm-associated infection caused by Staphylococcus epidermidis where polysaccharide intercellular adhesin (PIA) is a major mechanism of biofilm accumulation. PIA affects innate and humoral immunity in isolated cells and animal models. Few studies have examined these effects in prosthetic joint infection (PJI).
Methods: This study used ex vivo whole blood modelling in controls together with matched-serum and staphylococcal isolates from patients with PJI.
Results: Whole blood killing of PIA positive S. epidermidis and its isogenic negative mutant was identical. Differences were unmasked in immunosuppressed whole blood pre-treated with dexamethasone where PIA positive bacteria showed a more resistant phenotype. PIA expression was identified in three unique patterns associated with bacteria and leukocytes, implicating a soluble form of PIA. Purified PIA reduced whole blood killing while increasing C5a levels. In clinically relevant staphylococcal isolates and serum samples from PJI patients; firstly complement C5a was increased 3-fold compared to controls; secondly, the C5a levels were significantly higher in serum from PJI patients whose isolates preferentially formed PIA-associated biofilms.
Conclusions: These data demonstrate for the first time that the biological effects of PIA are mediated through C5a in patients with PJI.
Keywords: Biofilm; Complement C5a; Polysaccharide intercellular adhesin; Prosthetic joint infection; Staphylococcus epidermidis; Whole blood.
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