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Staphylococcus aureus internalization in mast cells in nasal polyps: Characterization of interactions and potential
Stephen M Hayes1, Timothy C Biggs1, Simon P Goldie1
1School of Clinical and Experimental Sciences, Faculty of Medicine, University of Southampton, Southampton, United Kingdom; Southampton NIHR Respiratory Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom; Department of Otorhinolaryngology/Head & Neck Surgery, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom; NIHR Wellcome Trust Clinical Research Facility, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom.
Background:
Chronic rhinosinusitis (CRS) with nasal polyps is a common chronic condition. The exact cause of nasal polyps remains unknown. Recently, we made the novel observation of intracellular localization of Staphylococcus aureus within mast cells in nasal polyps.
Objective:
This follow-up study aimed to further characterize interactions between S aureus and mast cells in this setting and elucidate potential internalization mechanisms with particular emphasis on the role of staphylococcal enterotoxin B (SEB).
Methods:
A prospective study was performed using an explant tissue model with ex vivo inferior turbinate mucosa obtained from patients with chronic rhinosinusitis with nasal polyps (n = 7) and patients without CRS (n = 5). Immunohistochemistry was used to characterize S aureus uptake into mast cells and investigate the effects of SEB on this process. An in vitro cell-culture model was used to investigate mast cell-S aureus interactions by using a combination of fluorescent in situ hybridization, confocal laser scanning microscopy, scanning electron microscopy, transmission electron microscopy, and proliferation assays.
Results:
S aureus was captured by extracellular traps and entered mast cells through phagocytosis. Proliferating intracellular S aureus led to the expansion and eventual rupture of mast cells, resulting in release of viable S aureus into the extracellular space. The presence of SEB appeared to promote internalization of S aureus into mast cells.
Conclusion:
This study provides new insights into the interactions between S aureus and mast cells, including the internalization process, and demonstrates a prominent role for SEB in promoting uptake of the bacteria into these cells.
Insights
Staphylococcus aureus enters and multiplies within mast cells in nasal polyps, causing cell rupture. Staphylococcal enterotoxin B (SEB) enhances this bacterial invasion, offering new insights into chronic rhinosinusitis with nasal polyps.
Area of Science:
- Immunology
- Microbiology
- Rhinology
Background:
- Chronic rhinosinusitis with nasal polyps (CRSwNP) is a prevalent condition with unknown etiology.
- A novel observation revealed intracellular Staphylococcus aureus within mast cells in nasal polyps.
Purpose of the Study:
- To further characterize Staphylococcus aureus and mast cell interactions in CRSwNP.
- To elucidate bacterial internalization mechanisms, focusing on staphylococcal enterotoxin B (SEB).
Main Methods:
- Ex vivo explant tissue model using inferior turbinate mucosa from CRSwNP and control patients.
- In vitro cell-culture models with advanced microscopy techniques (confocal, SEM, TEM) and FISH.
- Immunohistochemistry and proliferation assays to analyze bacterial uptake and mast cell responses.
Main Results:
- Staphylococcus aureus is captured by extracellular traps and internalized into mast cells via phagocytosis.
- Intracellular bacterial proliferation leads to mast cell expansion, rupture, and release of viable bacteria.
- Staphylococcal enterotoxin B (SEB) promotes the internalization of Staphylococcus aureus into mast cells.
Conclusions:
- This study elucidates novel insights into Staphylococcus aureus-mast cell interactions in CRSwNP.
- Demonstrates a significant role for SEB in enhancing bacterial uptake into mast cells.
- Highlights a potential mechanism contributing to the pathogenesis of CRSwNP.
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