title: Influenza virus A stimulates expression of eotaxin by nasal epithelial cells.
abstract: BACKGROUND
  Respiratory virus is one of the most common causes of airway inflammation, but its pathogenic mechanisms are not well understood. Eotaxin is a potent eosinophil chemoattractant and is a selective agonist for C-C chemokine 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.
  
  
  OBJECTIVE
  We hypothesized that eotaxin may play an important role in attracting inflammatory cells into the airway after viral infection and analysed whether viral infection induces eotaxin in nasal epithelial cells in vitro.
  
  
  METHODS
  Nasal epithelial cells obtained from polypectomy for nasal polyp were infected with influenza virus A (subtype H3N2). The cells and supernatants were collected 8, 24 and 48 h after infection. Eotaxin mRNA was analysed by RT-PCR. Eotaxin concentration in the supernatants was analysed by enzyme-linked immunosorbent assay. We also examined a blocking assay to analyse the intervention of pro-inflammatory cytokines, TNF-alpha and IL-1beta in eotaxin production induced by influenza virus.
  
  
  RESULTS
  The results showed that eotaxin was expressed constitutively in uninfected cells, but was up-regulated for both mRNA and protein levels in infected cells. Blocking experiments using anti-TNF-alpha and anti-IL-1beta antibodies showed no effects of these agents on the level of eotaxin. In addition, 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 important role in the pathogenesis of airway inflammation by inducing eotaxin.
authors: First Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan. mkawa@bellatlantic.net
authors: M
authors: M
authors: Kawaguchi
authors: F
authors: F
authors: Kokubu
authors: H
authors: H
authors: Kuga
authors: T
authors: T
authors: Tomita
authors: S
authors: S
authors: Matsukura
authors: H
authors: H
authors: Suzaki
authors: S K
authors: SK
authors: Huang
authors: M
authors: M
authors: Adachi
mesh_terms: D000906:Antibodies / Q000494:pharmacology; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines / Q000187:drug effects / Q000235:genetics* / Q000276:immunology / Q000494:pharmacology / Q000528:radiation effects; D004847:Epithelial Cells / Q000187:drug effects / Q000502:physiology*; D015870:Gene Expression; D006389:Hemagglutinins, Viral / Q000235:genetics / Q000528:radiation effects; D006801:Humans; D009980:Influenza A virus / Q000235:genetics*; D007251:Influenza, Human / Q000235:genetics; D007371:Interferon-gamma / Q000276:immunology / Q000494:pharmacology; D007375:Interleukin-1 / Q000276:immunology / Q000494:pharmacology; D009297:Nasal Mucosa / Q000166:cytology*; D012333:RNA, Messenger / Q000235:genetics / Q000528:radiation effects; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology / Q000494:pharmacology; D014466:Ultraviolet Rays
chemical_list: D000906:Antibodies; C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D016207:Cytokines; D006389:Hemagglutinins, Viral; D007375:Interleukin-1; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma