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Staphylococcus aureus , but not Staphylococcus epidermidis , modulates the oxidative response and induces apoptosis in human neutrophils
Author(s) -
NILSDOTTERAUGUSTINSSON ÅSA,
WILSSON ÅSA,
LARSSON JENNY,
STENDAHL OLLE,
ÖHMAN LENA,
LUNDQVISTGUSTAFSSON HELEN
Publication year - 2004
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2004.apm1120205.x
Subject(s) - staphylococcus epidermidis , microbiology and biotechnology , staphylococcus aureus , apoptosis , annexin , biology , p38 mitogen activated protein kinases , inflammation , immunology , oxidative stress , kinase , protein kinase a , bacteria , biochemistry , genetics
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.