Bacterial immune evasion via an IL-10 mediated host response, a novel pathophysiologic mechanism for chronic rhinosinusitis.

BACKGROUND

Staphylococcus aureus is a frequently implicated pathogen in chronic rhinosinusitis (CRS). S. aureus may promote commensalism by downregulating pro-inflammatory T cell host responses via an IL-10 mediated pathway. This finding, coupled with the observation that S. aureus and CD8+ T cell numbers are inversely correlated in CRS mucosa, suggests that S. aureus may evade immune destruction via IL-10 induction. To support this hypothesis, we evaluated i) whether IL-10 levels differ in CRS compared to controls (CTL) using microarray and immunohistochemistry and ii) whether IL-10 levels correlate with S. aureus and CD8+ T cell levels.

METHODOLOGY

Sinus epithelial brush samples from 12 patients undergoing ESS for CRS and 10 CTLs underwent microarray analysis of IL-10 gene expression. Microarray results were verified on simultaneously obtained surgical biopsy samples by immunohistochemistry staining for IL-10. Potential mechanisms were assessed by immunohistochemistry for CD8+ T cells and S. aureus.

RESULTS

IL-10 gene expression was significantly higher in CRS vs CTL subjects at the time of surgery. Immunohistochemistry confirmed increased levels of intraepithelial IL-10. A strong inverse correlation was observed between intraepithelial IL-10 and CD8+ T cell levels as was intraepithelial IL-10 and S. aureus.

CONCLUSION

Elevated IL-10 levels in sinus mucosa may be a potential pathophysiologic feature of CRS in association with a significant downregulation of host CD8+ T cell levels. While S. aureus is believed to play a role in IL-10 induction, a comparatively weaker relationship between S. aureus and IL-10 levels suggests other bacterial species may also induce IL-10 production as a common survival strategy in CRS.