ArticleJournal of innate immunity2012
The virulence regulator Agr controls the staphylococcal capacity to activate human neutrophils via the formyl peptide receptor 2.
Article in Journal of innate immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- Molecular Epidemiology Clinical Manifestations, Decolonization Strategies, and Treatment Options of Methicillin-ResistantPathogens (Basel, Switzerland) · 2025Review
- Staphylococcus epidermidis activates keratinocyte cytokine expression and promotes skin inflammation through the production of phenol-soluble modulins.Cell reports · 2023Article
- Article
- New insight into the virulence and inflammatory response ofFrontiers in cellular and infection microbiology · 2023Article
- Identification and characterization of the pathogenic potential of phenol-soluble modulin toxins in the mouse commensalFrontiers in immunology · 2022Article
- Phenol-Soluble Modulins FromFrontiers in cellular and infection microbiology · 2022Article
- Article
- One-carbon metabolism, folate, zinc and translation.Microbial biotechnology · 2020Article
- Inhibiting PSMα-induced neutrophil necroptosis protects mice with MRSA pneumonia by blocking the agr system.Cell death & disease · 2018Article
- Beyond sepsis: Staphylococcus epidermidis is an underestimated but significant contributor to neonatal morbidity.Virulence · 2018Review
- New Threats from an Old Foe: Methicillin-Resistant Staphylococcus aureus Infections in Neonates.Neonatology · 2018Review
- Formyl-peptide receptor 2 governs leukocyte influx in localFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Defining motility in the Staphylococci.Cellular and molecular life sciences : CMLS · 2017Review
- Pathogenic Mechanisms and Host Interactions inFrontiers in microbiology · 2017Review
- Phenol-soluble modulin α4 mediates Staphylococcus aureus-associated vascular leakage by stimulating heparin-binding protein release from neutrophils.Scientific reports · 2016Article
- Recognition of bacterial signal peptides by mammalian formyl peptide receptors: a new mechanism for sensing pathogens.The Journal of biological chemistry · 2015Article
- Enemy attraction: bacterial agonists for leukocyte chemotaxis receptors.Nature reviews. Microbiology · 2015Review
- The AgrD N-terminal leader peptide of Staphylococcus aureus has cytolytic and amyloidogenic properties.Infection and immunity · 2014Article
- Phenol-soluble modulins--critical determinants of staphylococcal virulence.FEMS microbiology reviews · 2014Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The Agr quorum-sensing system represents the master regulator for staphylococcal virulence factors and is known to have a strong impact on the release of pathogen-associated molecular pattern (PAMP) molecules. Among the various staphylococcal PAMPs, phenol-soluble modulin (PSM) peptides have attracted increasing interest because they are crucial for staphylococcal virulence and have neutrophil-recruiting properties. The latter depend on recognition of PSMs by the neutrophil formyl peptide receptor 2 (FPR2/ALX), for which PSMs are highly efficient agonists. We demonstrate that Agr inactivation in Staphylococcus aureus or S. epidermidis leads to strongly reduced neutrophil responses, which is in agreement with the previously reported strict control of PSM expression by Agr. Agr had a distinct and profound impact on activation of FPR2/ALX but not of the related FPR1 receptor that senses bacterial formylated peptides. S. epidermidis PSMs had similar FPR2/ALX-activating properties but differed in their dependence on N-terminal formylation compared to S. aureus PSMs. Moreover, S. aureus and S. epidermidis PSMs upregulated the neutrophil complement receptor CD11b via FPR2/ALX stimulation in an Agr-dependent fashion. Hence, Agr controls the capacity of staphylococcal pathogens to activate FPR2/ALX-dependent neutrophil responses, underscoring the crucial role of FPR2/ALX and PSMs in staphylococcus-host interaction.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.