Role of Staphylococcal Superantigens in Upper Airway Disease

Abstract and Introduction

Purpose of Review: Chronic rhinosinusitis with nasal polyps often represents a chronic severe inflammatory disease of the upper airways and may serve as a model for lower airway diseases such as late-onset intrinsic asthma. Enterotoxins derived from Staphylococcus aureus have been implicated in the pathophysiology of nasal polyps as disease-modifying factors; recent findings using therapeutic proof-of-concept approaches support this hypothesis.
Recent Findings: Nasal polyps (chronic rhinosinusitis with nasal polyps) are characterized by a T-helper-2 dominated cytokine pattern that includes interleukin-5 and formation of immunoglobulin E. This is in contrast to chronic rhinosinusitis without polyps, which exhibits T-helper-1 biased cytokine release. It is now evident that the cytokine environment is decisive regarding the impact of S. aureus derived enterotoxins, which function as superantigens. S. aureus enterotoxin B further shifts the cytokine pattern in nasal polyps toward T-helper-2 cytokines (increases greater than twofold for interleukin-2, interleukin-4 and interleukin-5), but it disfavours the T-regulatory cytokines interleukin-10 and transforming growth factor-β₁. Furthermore, S. aureus derived enterotoxins influence local immunoglobulin synthesis and induce polyclonal immunoglobulin E production, which may contribute to severe inflammation via activation of mast cells.
Summary: From this new understanding of chronic rhinosinusitis with nasal polyps, new therapeutic approaches emerge such as anti-interleukin-5, anti-immunoglobulin E, and antibiotic treatment. These may enlarge the nonsurgical armentarium.

Staphylococcal enterotoxins, as well as molecules derived from Streptococcus pyogenes and some viruses, are able to activate T cells via the T cell receptor-major histocompatibility complex class II complex, independent from the antigen-specific groove, by binding to the variable β-chain of the T cell receptor.^[1] The susceptibility of a T cell to those superantigens is therefore dependent on the usage of a specific β-chain repertoire, which leads to activation of abundant T cells in a given tissue. Once activated, T cells can orchestrate a severe inflammation, including polyclonal activation of B cells and recruitment of eosinophils (see for review^[2*]). Nasal polyp disease appears to be an excellent model in which to study superantigen-driven persistent airway disease.

Cite this: Role of Staphylococcal Superantigens in Upper Airway Disease - Medscape - Feb 01, 2008.

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