The Role of CC Chemokines in Chronic Sinusitis

Abstract

Chronic sinusitis is a complex disease with a substantial health care impact. Multiple factors play a role in the pathogenesis of this disease, but the initial process is still not well understood. Characteristic infiltrates of eosinophils are a hallmark of this disease. The selective appearance of T lymphocytes and eosinophils in growing polyps seems to be mediated by locally produced CC chemokines in cooperation with proinflammatory cytokines. Both are able to induce vascular adhesion molecules and attract rolling eosinophils as haptotaxins to the site of inflammation. Associated atopic diseases, like asthma or perennial allergies, have a higher eochemoattractant activity, which may contribute either to the nasal or bronchial mucosal accumulation of eosinophils. This could potentiate the eosinophilic effects in both tissues and possibly explain the severer symptomatology and higher recurrence rate of nasal polyps. RANTES, eotaxins 1 and 2 and IL-5 certainly play a role in chronic sinusitis. To our mind, the exact part of each mediator does not seem to be important, because just the complex cooperation of chemokines and also cytokines allows the underlying inflammatory process to become a chronic sinusitis. Therapeutic targets for eosinophil-related diseases are the impairment of CC chemokine expression and release by glucocorticoids, proteolytic degradation by endogenous enzymes, inhibition/antagonism of the CCR-3 and also endogenous antagonism by other chemokines.