AI Article Synopsis
- Staphylococcus aureus evades the immune response through toxins called γ-haemolysins (HlgAB and HlgCB), which are found in most human strains of the bacteria.
- These toxins target specific receptors on immune cells, with HlgAB affecting chemokine receptors and HlgCB targeting complement receptors, indicating a strategic method of immune evasion.
- In mouse models, HlgAB has been shown to promote S. aureus infection by interacting with the CCR2 receptor, highlighting the significant role of inflammatory macrophages in the infection process.
Article Abstract
Evasion of the host phagocyte response by Staphylococcus aureus is crucial to successful infection with the pathogen. γ-haemolysin AB and CB (HlgAB, HlgCB) are bicomponent pore-forming toxins present in almost all human S. aureus isolates. Cellular tropism and contribution of the toxins to S. aureus pathophysiology are poorly understood. Here we identify the chemokine receptors CXCR1, CXCR2 and CCR2 as targets for HlgAB, and the complement receptors C5aR and C5L2 as targets for HlgCB. The receptor expression patterns allow the toxins to efficiently and differentially target phagocytic cells. Murine neutrophils are resistant to HlgAB and HlgCB. CCR2 is the sole murine receptor orthologue compatible with γ-haemolysin. In a murine peritonitis model, HlgAB contributes to S. aureus bacteremia in a CCR2-dependent manner. HlgAB-mediated targeting of CCR2(+) cells highlights the involvement of inflammatory macrophages during S. aureus infection. Functional quantification identifies HlgAB and HlgCB as major secreted staphylococcal leukocidins.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4228697 | PMC |
| http://dx.doi.org/10.1038/ncomms6438 | DOI Listing |
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