Description:
<jats:title>Abstract</jats:title>
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<jats:title>Background</jats:title>
<jats:p>Polymorphonuclear neutrophil granulocytes (PMN) are phagocytes of the first line of antimicrobial defense. Previously we demonstrated that lipoteichoic acid (LTA) from <jats:italic>Staphylococcus aureus</jats:italic> (<jats:italic>S. aureus</jats:italic>) directly activates neutrophil granulocytes. Others have reported that exposure of <jats:italic>S. aureus</jats:italic> to β-lactam antibiotics leads to LTA release. In the present study we addressed the question whether exposure of <jats:italic>S. aureus</jats:italic> to β-lactam antibiotics or antibiotics of other groups results in the generation of PMN-stimulating activity and whether this activity can be attributed to LTA.</jats:p>
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<jats:title>Methods</jats:title>
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<jats:italic>S. aureus</jats:italic> were exposed to flucloxacillin, a β-lactam antibiotic or to the protein synthesis-inhibitors erythromycin and gentamicin, or to ciprofloxacin, a gyrase inhibitor. Supernatants of the antibiotic-treated bacteria were assayed for their LTA content and for their effect on PMN functions.</jats:p>
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<jats:title>Results</jats:title>
<jats:p>We observed that exposure of <jats:italic>S. aureus</jats:italic> to flucloxacillin and, to a lesser degree to ciprofloxacin, but not to erythromycin or gentamicin led to LTA release. Co-incubation of neutrophil granulocytes with LTA-containing supernatants led to PMN activation as assed by morphological changes, release of IL-8, delay of spontaneous apoptosis and enhanced phagocytic activity. Depletion of LTA from the supernatants markedly reduced their PMN-activating capacity.</jats:p>
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<jats:title>Conclusion</jats:title>
<jats:p>The findings suggest that, via the activation of PMN, antibiotic-induced LTA release from <jats:italic>S. aureus</jats:italic> leads to enhanced antimicrobial activity of the innate immune defense mechanisms.</jats:p>
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