title: Expression of eotaxin by normal airway epithelial cells after influenza virus A infection.
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-alpha and anti-IL-1beta 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.
authors.affiliation: First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan. mkawa@bellatlantic.net
authors.forename: M
authors.initials: M
authors.lastname: Kawaguchi
authors.forename: F
authors.initials: F
authors.lastname: Kokubu
authors.forename: H
authors.initials: H
authors.lastname: Kuga
authors.forename: T
authors.initials: T
authors.lastname: Tomita
authors.forename: S
authors.initials: S
authors.lastname: Matsukura
authors.forename: M
authors.initials: M
authors.lastname: Kadokura
authors.forename: M
authors.initials: M
authors.lastname: Adachi
mesh_terms: D001980:Bronchi / Q000378:metabolism* / Q000821:virology; D002478:Cells, Cultured; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000096:biosynthesis* / Q000235:genetics; D004847:Epithelial Cells / Q000378:metabolism / Q000821:virology; D019267:Hemagglutinin Glycoproteins, Influenza Virus / Q000235:genetics; D006801:Humans; D009980:Influenza A virus / Q000502:physiology*; D007375:Interleukin-1 / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D019267:Hemagglutinin Glycoproteins, Influenza Virus; D007375:Interleukin-1; D016328:NF-kappa B; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha