51. Expression of Eotaxin by Normal Airway Epithelial Cells after Influenza Virus A Infection
- Author
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Fumio Kokubu, Mio Kawaguchi, Hideki Kuga, Satoshi Matsukura, Mitsuru Adachi, Takeshi Tomita, and Mitsutaka Kadokura
- Subjects
Chemokine CCL11 ,Eotaxin ,Chemokine ,Immunology ,CCR3 ,Orthomyxoviridae ,Bronchi ,Hemagglutinin Glycoproteins, Influenza Virus ,Inflammation ,Proinflammatory cytokine ,immune system diseases ,medicine ,Humans ,Immunology and Allergy ,RNA, Messenger ,Cells, Cultured ,biology ,Tumor Necrosis Factor-alpha ,NF-kappa B ,Epithelial Cells ,hemic and immune systems ,General Medicine ,respiratory system ,biology.organism_classification ,respiratory tract diseases ,Influenza A virus ,Cell culture ,Chemokines, CC ,biology.protein ,Cytokines ,medicine.symptom ,CC chemokine receptors ,Interleukin-1 - Abstract
Background: Viral infection is known to cause lung inflammatory disease, including 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 receptor 3 (CCR3). CCR3 is expressed on eosinophils, basophils and T lymphocytes. These cells are known to be key cells in the pathogenesis of asthma. Although it has recently been demonstrated that airway epithelial cells express eotaxin in vivo and in vitro, there are few data about its epxression in viral infection. We hypothesized that eotaxin may play an important role in attracting inflammatory cells to the airways after viral infection, and analyzed whether viral infection attracts eotaxin in bronchial epithelial cells 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-polymerase chain reaction. Eotaxin protein levels in the culture media were analyzed 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 infected cells. Eotaxin protein release into culture media significantly increased after infection. Anti-TNF-α and anti-IL-1β antibodies did not alter the eotaxin protein levels after viral infection. Conclusions: These results suggest that influenza virus A infection in airway epithelial cells activates 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.
- Published
- 2000