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.

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We here demonstrate that mucosal IgE abs in NP tissue are functional and able to activate mast cells; specific IgE abs in NP tissue can be found independently of their presence in serum. We postulate that superantigen-induced polyclonal IgE in airway disease contributes to chronic inflammation by continuously activating mast cells.

Chronic rhinosinusitis is a heterogeneous group of chronic sinus diseases that may consist of clearly different disease entities. Further investigation of the pathomechanisms of chronic rhinosinusitis and the introduction of appropriate disease markers have recently facilitated disease classification. Evaluation of inflammatory cell profiles, the differentiation of T-effector cells, characterization of remodeling processes such as fibrosis or edema formation, and innate or adaptive immunity products such as Toll-like receptors and immunoglobulins all provide tools to identify distinct disease entities within the group of chronic sinus diseases. This disease differentiation will not only increase our knowledge of the pathophysiology of sinusitis but may lead to new diagnostic and therapeutic strategies specifically targeted and adapted to the diagnosed disease entity.

The role played by sinus disease in asthma is only partially understood, largely because of deficits in the clinical classification and in basic knowledge of pathophysiological pathways. Recent research into upper airway and sinus inflammation and remodelling may reveal new perspectives and lead to a classification of sinus disease, which will facilitate appropriate clinical and epidemiological studies.