title: Elevated macrophage inflammatory protein 1α and interleukin-17 production in an experimental asthma model infected with respiratory syncytial virus.
abstract: BACKGROUND
  Respiratory syncytial virus (RSV) infection is associated with both the development and exacerbation of bronchial asthma. We examined eosinophil infiltration and the cytokine profiles of both airway and peripheral blood in antigen-sensitized mice infected with RSV to investigate the pathogenesis of exacerbations of asthma due to RSV infection.
  
  
  METHODS
  Ovalbumin (OVA)-sensitized mice were challenged by OVA inhalation 3 times and then infected with RSV [10(5) TCID50 (50% of tissue culture infectious dose)/25 g body weight] or mock infection immediately after the last challenge. Animals from each group, namely, the control (PBS instead of OVA inhalation plus mock infection), RSV (PBS plus RSV), OVA (OVA plus mock) and OVA/RSV (OVA plus RSV) were analyzed. Analysis included evaluation of airway responsiveness to methacholine, pathological findings in the airway by hematoxylin and eosin (HE) and Luna staining, bronchoalveolar fluid (BALF) and peripheral leukocytes counts, and concentrations of multiple cytokines/chemokines in both BALF and serum.
  
  
  RESULTS
  Airway responsiveness was significantly enhanced in the OVA and OVA/RSV groups compared with the control group. Levels of tissue and BALF eosinophils were higher in the OVA and OVA/RSV groups than in the RSV or control group. Significantly higher levels of macrophage inflammatory protein (MIP)-1α in BALF were observed in the OVA/RSV group compared with the 3 other groups. Production of serum IL-17 was also significantly elevated in the OVA/RSV group compared with the control or OVA group.
  
  
  CONCLUSIONS
  These findings suggest that MIP-1α and IL-17 may play important roles in acute exacerbation of asthma induced by RSV in an animal model.
authors.affiliation: Department of Allergy and Immunology, Gunma Children's Medical Center, Shibukawa, Japan.
authors.forename: Taisei
authors.initials: T
authors.lastname: Ishioka
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Yamada
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Kimura
authors.forename: Masakazu
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Tsukagoshi
authors.forename: Kunihisa
authors.initials: K
authors.lastname: Kozawa
authors.forename: Kenichi
authors.initials: K
authors.lastname: Maruyama
authors.forename: Yasuhide
authors.initials: Y
authors.lastname: Hayashi
authors.forename: Masahiko
authors.initials: M
authors.lastname: Kato
mesh_terms: D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000276:immunology* / Q000821:virology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology / Q000276:immunology; D002460:Cell Line; D054405:Chemokine CCL3 / Q000096:biosynthesis*; D016207:Cytokines / Q000096:biosynthesis; D007073:Immunoglobulin E / Q000097:blood / Q000276:immunology; D020381:Interleukin-17 / Q000096:biosynthesis*; D008168:Lung / Q000276:immunology / Q000473:pathology / Q000821:virology; D008297:Male; D051379:Mice; D010047:Ovalbumin / Q000276:immunology; D018357:Respiratory Syncytial Virus Infections / Q000276:immunology* / Q000378:metabolism; D012136:Respiratory Syncytial Viruses / Q000276:immunology*
chemical_list: D000485:Allergens; D054405:Chemokine CCL3; D016207:Cytokines; D020381:Interleukin-17; D007073:Immunoglobulin E; D010047:Ovalbumin