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Published on: September 8, 2021
Staphylococcus aureus enterotoxin B disrupts nasal epithelial barrier integrity
Katleen Martens1,2, Sven F Seys1, Yeranddy A Alpizar3,4
1KU Leuven Department of Microbiology, Immunology and Transplantation, Allergy and Clinical Immunology Research Unit, Leuven, Belgium.
Staphylococcus aureus enterotoxin B (SEB) damages nasal polyp epithelial cells by activating Toll-like receptor 2 (TLR2) in chronic rhinosinusitis with nasal polyps (CRSwNP). Targeting TLR2 may reduce S. aureus-induced inflammation in CRSwNP.
Area of Science:
- Immunology
- Cell Biology
- Otorhinolaryngology
Background:
- Staphylococcus aureus colonization and enterotoxin B (SEB) are linked to severe chronic rhinosinusitis with nasal polyps (CRSwNP).
- The pathogenic mechanisms of SEB on epithelial barriers remain largely unexplored.
Purpose of the Study:
- To investigate the effect of SEB on nasal epithelial barrier function in CRSwNP.
Main Methods:
- Apical administration of SEB to air-liquid interface (ALI) cultures of primary nasal polyp epithelial cells and healthy controls.
- Evaluation of epithelial cell integrity and tight junction expression.
- In vitro and in vivo studies using Toll-like receptor 2 (TLR2) antagonism and tlr2 knockout mice.
Main Results:
- SEB decreased epithelial cell integrity and tight junction protein expression (occludin, ZO-1) in polyp cells.
- TLR2 antagonism prevented SEB-induced barrier disruption.
- SEB increased mucosal permeability and decreased occludin/ZO-1 mRNA in control mice, but not in tlr2 knockout mice.
- SEB induced IL-6 and IL-8 production, which was blocked by TLR2 antagonism.
Conclusions:
- SEB damages nasal polyp epithelial cell integrity by triggering TLR2 in CRSwNP.
- SEB may drive disease exacerbation rather than cause primary epithelial defects in CRSwNP.
- Interfering with TLR2 may mitigate S. aureus-induced inflammation in CRSwNP.
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