Staphylococcus epidermidis from prosthetic joint infections induces lower IL-1β release from human neutrophils than isolates from normal flora

Abstract

The aim of this study was to test the hypothesis that Staphylococcus epidermidis isolated from prosthetic joint infections (PJIs) differs from S. epidermidis isolated from normal flora in terms of its capacity to induce activation of caspase-1 and release of IL-1β in human neutrophils. The amount of active caspase-1 was determined over 6 h by detecting Ac-YVAD-AMC fluorescence in human neutrophils incubated with S. epidermidis isolates from PJIs (ST2) or normal flora. The amount of IL-1β was detected by ELISA in neutrophil supernatants after 6 h of incubation. Mean IL-1β release was lower after incubation with S. epidermidis from PJIs compared to isolates from normal flora, but no statistically significant difference was found in active caspase-1. Substantial inter-individual differences in both active caspase-1 and IL-1β were noted. These results suggest that evasion of innate immune response, measured as reduced capacity to induce release of IL-1β from human neutrophils, might be involved in the predominance of ST2 in S. epidermidis PJIs, but that other microbe-related factors are probably also important.

Keywords: Staphylococcus epidermidis; caspase-1; host-pathogen interactions/immunology; interleukin-1beta; prosthesis-related infections/pathology.