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Human formyl peptide receptor 2 senses highly pathogenic Staphylococcus aureus.

Abstract：

:Virulence of emerging community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) and other highly pathogenic S. aureus strains depends on their production of phenol-soluble modulin (PSM) peptide toxins, which combine the capacities to attract and lyse neutrophils. The molecular basis of PSM-stimulated neutrophil recruitment has remained unclear. Here, we demonstrate that the human formyl peptide receptor 2 (FPR2/ALX), which has previously been implicated in control of endogenous inflammatory processes, senses PSMs at nanomolar concentrations and initiates proinflammatory neutrophil responses to CA-MRSA. Specific blocking of FPR2/ALX or deletion of PSM genes in CA-MRSA severely diminished neutrophil detection of CA-MRSA. Furthermore, a specific inhibitor of FPR2/ALX and of its functional mouse counterpart blocked PSM-mediated leukocyte infiltration in vivo in a mouse model. Thus, the innate immune system uses a distinct FPR2/ALX-dependent mechanism to specifically sense bacterial peptide toxins and detect highly virulent bacterial pathogens. FPR2/ALX represents an attractive target for new anti-infective or anti-inflammatory strategies.

journal_name

Cell Host Microbe

journal_title

Cell host & microbe

authors

Kretschmer D,Gleske AK,Rautenberg M,Wang R,Köberle M,Bohn E,Schöneberg T,Rabiet MJ,Boulay F,Klebanoff SJ,van Kessel KA,van Strijp JA,Otto M,Peschel A

doi

10.1016/j.chom.2010.05.012

subject

Has Abstract

pub_date

2010-06-25 00:00:00

pages

463-73

issue

6

eissn

1931-3128

issn

1934-6069

pii

S1931-3128(10)00175-7

journal_volume

7

pub_type

杂志文章

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