Decreased expression of type I (IFN-β) and III interferon (IFN-λ) and IFN-stimulated genes in chronic rhinosinusitis with and without nasal polyps

Abstract Background Little is known about the antiviral responses in the sinonasal mucosa of patients with chronic rhinosinusitis (CRS). Objective we investigated the presence of virus, the expression of TLR3 and TLR7, and interferon (IFN) and IFN-stimulated genes (ISGs) in healthy mucosa of control and inflammatory sinus mucosa of CRS patients, and evaluated whether the levels of IFN and ISGs may be affected by CRS-related cytokines and by the treatment with macrolides, dexamethasone, or TLR3 and TLR7 agonists. Methods The presence of virus in sinonasal mucosa was evaluated with real time PCR. The expression of IFN and ISGs in sinonasal mucosa and in cultured epithelial cells treated with Th1 and Th2 cytokines, macrolides, dexamethasone, or TLR3 and TLR7 agonists were evaluated with real time PCR and western blot. The expression of TLR3 and TLR7 in sinonasal mucosa were evaluated with immunohistochemistry. Results Respiratory viruses was detected in 15 % of samples. IFN and ISGs are expressed in normal mucosa, but their levels were decreased in CRS patients. IFN and ISGs were up-regulated in cells treated with macrolides, dexamethasone, or TLR3 agonist, but a part of them was decreased in cytokine-treated cells. TLR3 and TLR7 levels showed no significant difference between normal and inflammatory sinus mucosa. Conclusion These results suggest that decreased levels of IFN and ISGs in CRS may contributes to the impairment of the antiviral innate response in inflammatory sinonasal epithelial cells. Macrolides and glucocorticoids may provide the positive effects on the treatment of CRS by upregulating IFN and ISGs.