β-lactam antibiotic-induced release of lipoteichoic acid from <it>Staphylococcus aureus </it>leads to activation of neutrophil granulocytes

<p>Abstract</p> <p>Background</p> <p>Polymorphonuclear neutrophil granulocytes (PMN) are phagocytes of the first line of antimicrobial defense. Previously we demonstrated that lipoteichoic acid (LTA) from <it>Staphylococcus aureus </it>(<it>S. aureus&l...

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Main Authors: Hartung Thomas (Author), Morath Siegfried (Author), Ziemann Christian (Author), Starke Andrea (Author), Lotz Sonja (Author), Solbach Werner (Author), Laskay Tamás (Author)
Format: Book
Published: BMC, 2006-06-01T00:00:00Z.
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Summary:<p>Abstract</p> <p>Background</p> <p>Polymorphonuclear neutrophil granulocytes (PMN) are phagocytes of the first line of antimicrobial defense. Previously we demonstrated that lipoteichoic acid (LTA) from <it>Staphylococcus aureus </it>(<it>S. aureus</it>) directly activates neutrophil granulocytes. Others have reported that exposure of <it>S. aureus </it>to β-lactam antibiotics leads to LTA release. In the present study we addressed the question whether exposure of <it>S. aureus </it>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.</p> <p>Methods</p> <p><it>S. aureus </it>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.</p> <p>Results</p> <p>We observed that exposure of <it>S. aureus </it>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.</p> <p>Conclusion</p> <p>The findings suggest that, via the activation of PMN, antibiotic-induced LTA release from <it>S. aureus </it>leads to enhanced antimicrobial activity of the innate immune defense mechanisms.</p>
Item Description:10.1186/1476-0711-5-15
1476-0711