Rhinovirus infection up-regulates eotaxin and eotaxin-2 expression in bronchial epithelial cells

Background Human rhinoviruses (RVs) are the most common precipitants of ast hma exacerbations. RV infection of bronchial epithelium results in local ai rway inflammation inducing eosinophil recruitment and activation. Induction of eosinophil chemoattractants could represent a central mechanism. as wel l as a prime target for intervention. Objective To assess the effect of RV infection on mRNA expression and produ ction of eosinophil chemoattractants by bronchial epithelial cells in-vitro . Methods BEAS-2B cells were infected with major and minor RVs and the mRNA e xpression of IL-8, RANTES, MIP-1 alpha, eotaxin, eotaxin-2, MCP-2, MCP-3 an d MCP-4 was assessed by reverse transcription PCR. In cases where mRNA indu ction was observed, a fluoroimmunoassay was used to confirm protein product ion. To assess the virus-specificity of the observed reactions. cells were also exposed to inactivated RVs. Results RV infection was able to up-regulate mRNA expression of IL-8, RANTE S, MIP-1 alpha. eotaxin and eotaxin-2, did not affect MCP-4. while MCP-2 an d MCP-3 were not expressed either at baseline or after virus infection. Pro tein production was confirmed for IL-8. RANTES and cotaxin. but not for MIP -1 alpha. When RVs were inactivated cytokine upregulation was almost comple tely lost. Conclusion Infection of bronchial epithelial cells with RVs results in the production of a wide array of mediators that are able to chemoattract eosin ophils. These include the eosinophil-specific molecules cotaxin and eotaxin -2, in addition to IL-8 and RANTES. which are the most abundant. Eosinophil recruitment after RV infection of bronchial epithelium could represent a c entral event in the pathogenesis of virus-induced asthma exacerbations.