Formyl peptide receptor-mediated proinflammatory consequences of peptide deformylase inhibition in Staphylococcus aureus

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• 作者：Diana Mader ; Marie-José ; phe Rabiet ; Francois Boulay ; Andreas Peschel
• 关键词：Staphylococcus aureus ; Actinonin ; Methionyl-tRNA formyltransferase ; Peptide deformylase ; Formyl peptide receptor ; Inflammation ; Chemotaxis ; IL-8
• 刊名：Microbes and Infection
• 出版年：2010
• 出版时间：May 2010
• 年：2010
• 卷：12
• 期：5
• 页码：415-419
• 全文大小：216 K

文摘

The biosynthesis of proteins with N-terminal formylated methionine residues and subsequent protein deformylation are unique and invariant bacterial processes. They are exploited by the capacity of the human innate immune system to sense formylated peptides (FPs) and targeted by the deformylation-blocking antibiotic actinonin. We show that human polymorphonuclear leukocytes respond via the formyl peptide receptor (FPR) with increased calcium ion fluxes, chemotactic migration, IL-8 release, and CD11b upregulation to the human pathogen Staphylococcus aureus upon actinonin treatment. These data underscore the crucial role of bacterial FPs in innate immunity and indicate that deformylase inhibition may have considerable proinflammatory consequences.