Formyl-Peptide Receptor Activation Enhances Phagocytosis of Community-Acquired Methicillin-Resistant Staphylococcus aureus
| Autor: | Christian Beck, Andreas Peschel, Elisabeth Weiß, Dorothee Kretschmer, Katja Schlatterer |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Methicillin-Resistant Staphylococcus aureus
0301 basic medicine Neutrophils Phagocytosis Fc receptor Macrophage-1 Antigen Blood Donors Complement receptor medicine.disease_cause Microbiology 03 medical and health sciences 0302 clinical medicine medicine Humans Immunology and Allergy Receptors Lipoxin Receptor Opsonin Cells Cultured Formyl peptide receptor biology Chemistry Interleukin-8 Receptors IgG Pattern recognition receptor Staphylococcal Infections Receptors Formyl Peptide Community-Acquired Infections 030104 developmental biology Infectious Diseases Staphylococcus aureus Receptors Pattern Recognition Receptors Complement 3b biology.protein 030215 immunology |
| Zdroj: | The Journal of Infectious Diseases. |
| ISSN: | 1537-6613 0022-1899 |
| DOI: | 10.1093/infdis/jiz498 |
| Popis: | BackgroundFormyl-peptide receptors (FPRs) are important pattern recognition receptors that sense specific bacterial peptides. Formyl-peptide receptors are highly expressed on neutrophils and monocytes, and their activation promotes the migration of phagocytes to sites of infection. It is currently unknown whether FPRs may also influence subsequent processes such as bacterial phagocytosis and killing. Staphylococcus aureus, especially highly pathogenic community-acquired methicillin-resistant S aureus strains, release high amounts of FPR2 ligands, the phenol-soluble modulins.MethodsWe demonstrate that FPR activation leads to upregulation of complement receptors 1 and 3 as well as FCγ receptor I on neutrophils and, consequently, increased opsonic phagocytosis of S aureus and other pathogens.ResultsIncreased phagocytosis promotes killing of S aureus and interleukin-8 release by neutrophils.ConclusionsWe show here for the first time that FPRs govern opsonic phagocytosis. Manipulation of FPR2 activation could open new therapeutic opportunities against bacterial pathogens. |
| Databáze: | OpenAIRE |
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