Nasal polyps in adults, characterized by abundant eosinophils, local overproduction of
immunoglobulin E, and often associated with
asthma, have been appreciated as an eosinophilic
inflammation, potentially of allergic origin, but unrelated to a bacterial impact. Evidence accumulates, however, that Staphylococcus aureus colonizes chronic
rhinosinusitis with, but not without
polyps, with significantly increased prevalence. The germs release
enterotoxins, which act as
superantigens and induce a topical multiclonal
IgE-formation as well as a severe, possibly
steroid-insensitive eosinophilic
inflammation. Recently, S. aureus could be demonstrated to reside intraepithelially, and potentially to release
superantigens into the tissue from within the epithelial cells. An immune defect, either in the innate or adaptive immunity, might be responsible for this phenomenon. Follicle-like structures and lymphocyte accumulations, specifically binding
enterotoxins, can be found within the
polyp tissues, giving rise to local
IgE formation. The
superantigen-induced immune response also leads to a modulation of the severity of the eosinophilic
inflammation, and may be linked to lower airway co-morbidity in
polyp patients. Interestingly,
IgE antibodies to
enterotoxins can be found in the majority of
aspirin-sensitive
polyp tissues, associated with a substantial increase in ECP and
IL-5. The possible role of S. aureus
enterotoxins in
polyp disease in Europe, the US and Asia has meanwhile been supported by several studies, demonstrating the presence of
IgE antibodies to
enterotoxins and inflammatory consequences in
nasal polyp tissue. First studies also point to an involvement of S. aureus derived
enterotoxins in lower airway disease, such as severe
asthma and exacerbated
COPD, clearly suggesting a clinical need for diagnosis and treatment of the germ and its related effects. Therapeutic approaches are so far empirical, and need further study, also serving to proof the clinical relevance of the concept.