[Cytokines and chemokines in paranasal sinus diseases]

New insights into inflammatory processes became possible by investigating the pattern of cytokines and chemokines as well as adhesion molecules in different acute and chronic sinus diseases since the last decade. This review aims to update and discuss findings of in vitro and in vivo studies concerning the role of cytokines and chemokines in inflammatory sinus diseases during the last years.

Discrepancies in research findings may be due to the small available databases today, the use of different techniques for investigation, and the lack of a valuable classification of sinus diseases. Despite this discrepancies, there is evidence that in acute bacterial and viral sinusitis, proinflammatory cytokines play a dominant role in initiating and sustaining the inflammation, which is especially characterized by neutrophil tissue infiltration. In chronic sinusitis IL-3 dominates the cytokine profile, giving support to a variety of inflammatory cells. IL-3 may also contribute to fibrosis and constant thickening of the mucosa leading to an obstruction of the ostiomeatal complex. In most bilateral nasal polyps, tissue eosinophilia is a striking finding which is believed to play a central role in pathogenesis, as it does in asthma. Eosinophilia may be explained by increased migration and prolonged eosinophil survival. Activation and survival of eosinophils in nasal polyps are thought to be regulated by autocrine stimulation by IL-5. Therefore, IL-5 represents the main target for future therapy in nasal polyposis.

Defining cytokine and chemokine patterns in inflammatory sinus diseases leads to a better understanding of immunologic processes in nasal mucosa. Results of cytokine and chemokine research are of paramount interest in developing new therapeutic approaches.