Expression of eotaxin by normal airway epithelial cells after influenza virus A infection

Background: Viral infection is known to cause lung inflammatory disease, in cluding bronchial asthma. The mechanisms of inflammatory cell accumulation into the airways after viral infection are not well understood. Eotaxin is a CC chemokine which is a potent and specific agonist for CC chemokine rece ptor 3 (CCR3). CCR3 is expressed on eosinophils, basophils and T lymphocyte s. These cells are known to be key cells in the pathogenesis of asthma. Alt hough it has recently been demonstrated that airway epithelial cells expres s eotaxin in vivo and in vitro, there are few data about its expression in viral infection. We hypothesized that eotaxin may play an important role in attracting inflammatory cells to the airways after viral infection, and an alyzed whether viral infection attracts eotaxin in bronchial epithelial cel ls in vitro. Methods: Human airway epithelial cells obtained from bronchial tissue at lobectomy for lung cancer were infected with influenza virus A ( subtype H3N2). The cells and cultured media were collected 8, 24, and 48 h after infection. Eotaxin mRNA was analyzed with reverse transcriptase-polym erase chain reaction. Eotaxin protein levels in the culture media were anal yzed by enzyme-linked immunosorbent assay. We also studied a blocking assay to analyze the intervention of proinflammatory cytokines in its production induced by influenza virus. Results: Eotaxin mRNA appeared to be expressed constitutively in uninfected cells but was expressed more clearly in infec ted cells. Eotaxin protein release into culture media significantly increas ed after infection. Anti-TNF-alpha and anti-IL-1 beta antibodies did not al ter the eotaxin protein levels after viral infection. Conclusions: These re sults suggest that influenza virus A infection in airway epithelial cells a ctivates the expression of eotaxin and that eotaxin may participate in the pathogenesis of airway inflammatory disease caused by viral infection, such as infectious type asthma. Copyright (C) 2000 S. Karger AG, Basel.