title: Staphylococcus aureus, but not Staphylococcus epidermidis, modulates the oxidative response and induces apoptosis in human neutrophils.
abstract: S. epidermidis is the most common isolate in foreign body infections. The aim of this study was to understand why S. epidermidis causes silent biomaterial infections. In view of the divergent inflammatory responses S. epidermidis and S. aureus cause in patients, we analyzed how they differ when interacting with human neutrophils. Neutrophils interacting with S. epidermidis strains isolated either from granulation tissue covering infected hip prostheses or from normal skin flora were tested by measuring the oxidative response as chemiluminescence and apoptosis as annexin V binding. Different S. aureus strains were tested in parallel. All S. epidermidis tested were unable to modulate the oxidative reaction in response to formyl-methionyl-leucyl-phenylalanine (fMLP) and did not provoke, but rather inhibited, apoptosis. In contrast, some S. aureus strains enhanced the oxidative reaction, and this priming capacity was linked to p38-mitogen-activated-protein-kinase (p38-MAPK) activation and induction of apoptosis. Our results may explain why S. epidermidis is a weak inducer of inflammation compared to S. aureus, and therefore responsible for the indolent and chronic course of S. epidermidis biomaterial infections.
authors.affiliation: Division of Infectious Diseases, Department of Molecular and Clinical Medicine, Linköping University, Linköping, Sweden. asa.nilsdotter@lio.se
authors.forename: Asa
authors.initials: A
authors.lastname: Nilsdotter-Augustinsson
authors.forename: Asa
authors.initials: A
authors.lastname: Wilsson
authors.forename: Jenny
authors.initials: J
authors.lastname: Larsson
authors.forename: Olle
authors.initials: O
authors.lastname: Stendahl
authors.forename: Lena
authors.initials: L
authors.lastname: Ohman
authors.forename: Helen
authors.initials: H
authors.lastname: Lundqvist-Gustafsson
mesh_terms: D017304:Annexin A5 / Q000378:metabolism; D017209:Apoptosis / Q000276:immunology*; D001672:Biocompatible Materials; D015153:Blotting, Western; D006801:Humans; D008163:Luminescent Measurements; D020928:Mitogen-Activated Protein Kinases / Q000276:immunology; D009504:Neutrophils / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D010587:Phagocytosis / Q000276:immunology; D016459:Prosthesis-Related Infections / Q000382:microbiology; D016897:Respiratory Burst / Q000276:immunology*; D013203:Staphylococcal Infections / Q000276:immunology / Q000382:microbiology*; D013211:Staphylococcus aureus / Q000276:immunology / Q000472:pathogenicity*; D013212:Staphylococcus epidermidis / Q000276:immunology / Q000472:pathogenicity*; D018709:Statistics, Nonparametric; D048051:p38 Mitogen-Activated Protein Kinases
chemical_list: D017304:Annexin A5; D001672:Biocompatible Materials; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases