ArticleCommunications biology2022
Phenol-soluble modulin α and β display divergent roles in mice with staphylococcal septic arthritis.
Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Microbe-Derived Antimicrobial Peptides: Immunomodulation and Gut Microbiota Homeostasis.Microorganisms · 2026Review
- Article
- Computational exploration of the self-aggregation mechanisms of phenol-soluble modulins β1 and β2 in Staphylococcus aureus biofilms.Colloids and surfaces. B, Biointerfaces · 2025Article
- Steamed panax notoginseng mitigates CA-MRSA USA300-induced necroptosis in human neutrophils.Frontiers in pharmacology · 2025Article
- Bacterial and host interactions inFrontiers in microbiology · 2025Review
- Utilization of In Vivo Imaging System to Study Staphylococcal Sepsis and Septic Arthritis Progression in Mouse Model.Pathogens (Basel, Switzerland) · 2024Article
- The role of Staphylococcus aureus quorum sensing in cutaneous and systemic infections.Inflammation and regeneration · 2024Review
- Exploring the role of bacterial virulence factors and host elements in septic arthritis: insights from animal models for innovative therapies.Frontiers in microbiology · 2024Review
- The Impact of Aging and Toll-like Receptor 2 Deficiency on the Clinical Outcomes of Staphylococcus aureus Bacteremia.The Journal of infectious diseases · 2023Article
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Phenol-soluble modulin α (PSMα) is identified as potent virulence factors in Staphylococcus aureus (S. aureus) infections. Very little is known about the role of PSMβ which belongs to the same toxin family. Here we compared the role of PSMs in S. aureus-induced septic arthritis in a murine model using three isogenic S. aureus strains differing in the expression of PSMs (Newman, Δpsmα, and Δpsmβ). The effects of PSMs on neutrophil NADPH-oxidase activity were determined in vitro. We show that the PSMα activates neutrophils via the formyl peptide receptor (FPR) 2 and reduces their NADPH-oxidase activity in response to the phorbol ester PMA. Despite being a poor neutrophil activator, PSMβ has the ability to reduce the neutrophil activating effect of PSMα and to partly reverse the effect of PSMα on the neutrophil response to PMA. Mice infected with S. aureus lacking PSMα had better weight development and lower bacterial burden in the kidneys compared to mice infected with the parental strain, whereas mice infected with bacteria lacking PSMβ strain developed more severe septic arthritis accompanied with higher IL-6 and KC. We conclude that PSMα and PSMβ play distinct roles in septic arthritis: PSMα aggravates systemic infection, whereas PSMβ protects arthritis development.
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