Nasal polyposis (NP) is a chronic inflammatory disease of the sinuses often associated with asthma. Although we have not yet achieved a full understanding of the precise mechanisms underlying the pathogenesis of NP, recent insights have been acquired into the regulation of eosinophil chemotaxis, activation, and survival, in addition to their possible link to gross histopathologic changes such as pseudocyst formation. Interleukin (IL)-5, transforming growth factor-beta(1), and eotaxin seem to be crucial players in the regulation of eosinophilic inflammation and extracellular matrix breakdown. The cytokine pattern in NP assumes neither a T helper 1 (Th1) nor Th2 type predominance, because IL-4, IL-5, IL-12, and interferon-gamma have all been shown to be upregulated in NP tissue, without influence of the atopic status. However, recent studies have demonstrated a strong local upregulation of the immunoglobulin E (IgE) synthesis with the formation of specific IgE to Staphylococcus aureus enterotoxins, suggesting a possible role of superantigens in these pathologic processes.