title: The soluble tumor necrosis factor-alpha receptor suppresses airway inflammation in a murine model of acute asthma.
abstract: OBJECTIVE
  Tumor necrosis factor-alpha (TNF-alpha) is a proinflammatory cytokine that has been implicated in many aspects of the airway pathology in asthma. TNF-alpha blocking strategies are now being tried in asthma patients. This study investigated whether TNF-alpha blocking therapy inhibits airway inflammation and airway hyperresponsiveness (AHR) in a mouse model of asthma. We also evaluated the effect of TNF-alpha blocking therapy on cytokine production and adhesion molecule expression.
  
  
  METHODS
  Ovalbumin (OVA) sensitized BALB/c female mice were exposed to intranasal OVA administration on days 31, 33, 35, and 37. Mice were treated intraperitoneally with soluble TNF-alpha receptor (sTNFR) during the OVA challenge.
  
  
  RESULTS
  There were statistically significant decreases in the numbers of total cell and eosinophil in bronchoalveolar lavage fluid (BALF) in the sTNFR treated group compared with the OVA group. However, sTNFR-treatment did not significantly decrease AHR. Anti-inflammatory effect of sTNFR was accompanied with reduction of T helper 2 cytokine levels including interleukin (IL)-4, IL-5 and IL-13 in BALF and vascular cell adhesion molecule 1 expression in lung tissue.
  
  
  CONCLUSIONS
  These results suggest that sTNFR treatment can suppress the airway inflammation via regulation of Th2 cytokine production and adhesion molecule expression in bronchial asthma.
authors.affiliation: Division of Pulmonology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
authors.forename: Hae-Seong
authors.initials: HS
authors.lastname: Nam
authors.forename: Sook Young
authors.initials: SY
authors.lastname: Lee
authors.forename: Seung Jun
authors.initials: SJ
authors.lastname: Kim
authors.forename: Ju Sang
authors.initials: JS
authors.lastname: Kim
authors.forename: Soon Seog
authors.initials: SS
authors.lastname: Kwon
authors.forename: Young Kyoon
authors.initials: YK
authors.lastname: Kim
authors.forename: Kwan Hyung
authors.initials: KH
authors.lastname: Kim
authors.forename: Hwa Sik
authors.initials: HS
authors.lastname: Moon
authors.forename: Jeong Sup
authors.initials: JS
authors.lastname: Song
authors.forename: Sung Hak
authors.initials: SH
authors.lastname: Park
authors.forename: Seok Chan
authors.initials: SC
authors.lastname: Kim
mesh_terms: D000818:Animals; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000188:drug therapy* / Q000276:immunology*; D015153:Blotting, Western; D001980:Bronchi / Q000187:drug effects; D016535:Bronchial Hyperreactivity; D001992:Bronchoalveolar Lavage Fluid / Q000276:immunology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D007150:Immunohistochemistry; D007249:Inflammation / Q000188:drug therapy*; D018793:Interleukin-13 / Q000378:metabolism; D015847:Interleukin-4 / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000627:therapeutic use*
chemical_list: D018927:Anti-Asthmatic Agents; D018793:Interleukin-13; D015848:Interleukin-5; D014409:Tumor Necrosis Factor-alpha; D015847:Interleukin-4; D010047:Ovalbumin