Adaptive immuneresponses in Staphylococcusaureus biofilm–associated chronic rhinosinusitis.

Allergy 2011; DOI: 10.1111/j.1398-9995.2011.02678.x

Foreman A., Holtappels G., Psaltis A.J.,Jervis-Bardy J., Field J., Wormald P.-J., Bachert C.

Abstract

Background:  The etiopathogenesis of chronic rhinosinusitis (CRS) iscurrently an area of intense debate. Recently, biofilms have been proposed as apotential environmental trigger in this disease. In particular, Staphylococcusaureus biofilms appear to be a predictor of severedisease recalcitrant to current treatment paradigms. However, direct causallinks between biofilms and host immune activation are currently lacking. Thisstudy aimed to document both the adaptive immune responses that characterize S.aureus biofilm–associated CRS and the relativecontributions of staphylococcal superantigens and S.aureus biofilms in the inflammatory make-up of this disease.

Methods:  A total of 53 disease subjects and 15 controls wererecruited. Sinonasal mucosa was collected for the determination ofS.aureus and Haemophilus influenzae biofilms and presence of total and superantigen-specific IgEand for the measurement of cytokines that characterize the T-helper pathways.

Results: Staphylococcusaureus biofilms and superantigens are significantlyassociated in CRS patients, suggesting the biofilm may be a nidus forsuperantigen-eluting bacteria. The presence of S.aureus biofilms is associated with eosinophilicinflammation, across the spectrum of CRS, on the back of a T-helper2 skewing of the host’s adaptive immune response (elevated EosinophilicCationic Protein and IL-5). This can be distinguished from the superantigeniceffect resulting in the induction of IgE.

Conclusion:  This study provides novel evidence of a link between S.aureus biofilms and skewing of the T-cell responsetoward the T-helper2 pathway that is independent of superantigen activities.Further research is required to confirm the cause–effect relationship of thisassociation.