Influenza virus A stimulates expression of eotaxin by nasal epithelial cells

Background Respiratory virus is one of the most common causes of airway inf lammation, but its pathogenic mechanisms are not well understood. Eotaxin i s a potent eosinophil chemoattractant and is a selective agonist for C-C ch emokine receptor 3 (CCR3). Although it has recently been demonstrated that epithelial cells express eotaxin, both in vivo and in vitro, there are few data concerning the expression in viral infection. Objects We hypothesized that eotaxin may play an important role in attracti ng inflammatory cells into the airway after viral infection and analysed wh ether viral infection induces eotaxin in nasal epithelial cells in vitro. Methods Nasal epithelial cells obtained from polypectomy for nasal polyp we re infected with influenza virus A (subtype H3N2). The cells and supernatan ts were collected 8, 24 and 48 h after infection. Eotaxin mRNA was analysed by RT-PCR. Eotaxin concentration in the supernatants was analysed by enzym e-linked immunosorbent assay. We also examined a blocking assay to analyse the intervention of pro-inflammatory cytokines, TNF-alpha and IL-1 beta in eotaxin production induced by influenza virus. Results The results showed that eotaxin was expressed constitutively in uni nfected cells, but was up-regulated for both mRNA and protein levels in inf ected cells. Blocking experiments using anti-TNF-alpha and anti-IL-1 beta a ntibodies showed no effects of these agents on the level of eotaxin. In add ition, UV-inactivated virus did not enhance the expression of eotaxin. Conclusions These results suggest that influenza virus A infection in nasal epithelial cells stimulates the expression of eotaxin, and may play an imp ortant role in the pathogenesis of airway inflammation by inducing eotaxin.