Most cases of acute sinusitis are thought to follow viral upper respiratory tract infections URIs , of those URIs being caused by rhinovirus RV . Approximately . -. of patients suffering from viral URIs develop acute bacterial rhinosinusitis. If left untreated, acute bacterial rhinosinusitis may cause severe complications and/or become chronic paranasal sinusitis. In contrast to the association of RV with acute sinusitis, little is known about the role of RV infections in the pathogenesis of

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... onic sinusitis. In addition, it is unclear if RV acts only as a triggering event for acute sinusitis, which then leads to subsequent development of chronic sinusitis, or if RV persists in the mucosae of chronic sinusitis patients and plays an active role in the disease process. To understand the potential role of RV in the pathogenesis of chronic sinusitis, the author investigated pathogenetic role of RV in chronic sinusitis. In this lecture, important research finding studied in my lab will be presented. First, we detected RV in of turbinate epithelial cell samples from chronic sinusitis patients but in none of the control samples. Our detection of virus in several mucosal scrapings may be caused by a subclinical persistence of RV from previous infections. These findings suggest that a subclinical infection of turbinate epithelial cells by RV may be significant in the pathogenesis of chronic sinusitis, in a manner similar to those reported in asthma and otitis media with effusion. Second, we showed that RV-infection of HNEC signifi cantly increases the gene and protein expression of three types of cell adhesion molecules including Fn, PAF-r, and CEACAM. These cell adhesion molecules are involved in the adhesion of major pathogenic bacteria to host cells. This finding suggests that the enhanced expression of Fn, PAF-r, and CEACAM following RV-infection may increase the level of adhesion of S. aureus, S. pneumoniae, and H. influenzae, the most common causative pathogens of bacterial rhinosinusitis RS , to HNEC. These findings provide the basis for understanding the causal relationship between rhinovirus infection and secondary bacterial RS. Third, we demonstrated that RV infection of cultured nasal epithelial cell monolayers decreased the expression of the TJ components claudin-, occludin, and ZO-, and the major AJ component E-cadherin. Importantly, these decreases were associated with functional changes in epithelial barrier function, as evidenced by a decrease in TER. The results of our in vitro study are consistent with the idea that RV infection in nasal epithelial cells aggravates mucus production, vascular permeability, and secondary bacterial infection of the airway epithelium by attenuating barrier function, as suggested by previous studies. Fourth, we also found that RV-infection significantly enhanced the expression of MMP-, MMP-, and VEGF in NP fibroblasts. These in vitro findings suggest that RV infection may contribute to the pathogenesis of NP formation in patients with CRSwNP. Lastly, we showed that fungal exposure of the NPECs, with or without rhinovirus infection, did not induce the production of IL-from eosinophils; however, the NPECs with rhinovirus infection induced the production of TNF-_ from eosinophils with . The results of this study demonstrate that fungi and rhinovirus induced cytokine production in primary NPECs. In addition, we also foud that there might be some synergism between rhinovirus infection and airborne fungal exposure enhancing the cytokine production of airway epithelial cells. There was some synergism between rhinovirus infections and air-borne fungal exposure that enhanced the migration of eosinophils. Taken together, rhinovirus seem to have significant role in the pathogenesis of chronic sinusitis.