Open AccessThe capacity of bovine endothelial cells to eliminate intracellular Staphylococcus aureus and Staphylococcus epidermidis is increased by the proinflammatory cytokines TNF‐α and IL‐1β
Author(s) -
OviedoBoyso Javier,
CardosoCorrea Bernardo I.,
CajeroJuárez Marcos,
BravoPatiño Alejandro,
ValdezAlarcón Juan J.,
BaizabalAguirre Víctor M.
Publication year - 2008
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2008.00447.x
Subject(s) - staphylococcus aureus , microbiology and biotechnology , proinflammatory cytokine , staphylococcus epidermidis , biology , staphylococcal infections , intracellular , intracellular parasite , tumor necrosis factor alpha , immunology , bacteria , inflammation , genetics
Staphylococcus aureus is a pathogenic bacterium causing clinical and subclinical bovine mastitis. Infections of the udder by S. aureus are frequently associated with the presence of Staphylococcus epidermidis , an opportunistic pathogen. We reported previously that the capacity of bovine endothelial cells (BEC) to endocytize S. aureus is associated with the activation of NF‐κB and modulated by the proinflammatory cytokines TNF‐α and IL‐1β. In this work, we explore the ability of BEC to eliminate intracellular S. aureus and S. epidermidis and their response to these cytokines. Time‐kinetics survival experiments indicated that BEC eliminate intracellular S. epidermidis more efficiently. Replication of S. aureus , but not S. epidermidis , inside BEC was evident by an increase in intracellular bacteria recovered at 2 h postinfection. Afterwards, the intracellular number of staphylococci decreased gradually, reaching the lowest value at 24 h. Treatment of BEC with TNF‐α or IL‐1β potentiated the capacity of BEC to eliminate both Staphylococcus species at the times tested. These results indicate that activation of the intrinsic antistaphylococcal response in BEC, enhanced by TNF‐α and IL‐1β, is effective to eliminate S. aureus and S. epidermidis and suggest that endothelial cells may play a prominent role in the defense against infections caused by these bacteria.