title: Anti-tumor necrosis factor-alpha treatment reduces allergic responses in an allergic rhinitis mouse model.
abstract: BACKGROUND
  Tumor necrosis factor (TNF)-α is a principal mediator of the acute inflammatory response, including allergic rhinitis. TNF-α inhibitors are widely used for the treatment of inflammatory conditions such as rheumatoid arthritis and inflammatory bowel diseases; however, the effects of TNF-α inhibitors on allergic rhinitis are not well established. We aimed to investigate the effects of infliximab, a TNF-α inhibitor, on allergic rhinitis in a mouse model.
  
  
  METHODS
  BALB/c mice were sensitized with ovalbumin (OVA) and alum, and challenged intranasally with OVA. The TNF-α inhibitor, infliximab was administered intraperitoneally, and multiple parameters of allergic responses were evaluated to determine the effects of infliximab.
  
  
  RESULTS
  Infliximab reduced allergic symptoms and eosinophilic infiltration into the nasal mucosa. It also suppressed total and OVA-specific IgE levels, and inhibited local Th2 cytokine transcription in the nasal mucosa and systemic Th2 cytokine production by splenocytes. Furthermore, the expression of E-selectin, neither intercellular adhesion molecule 1 (ICAM-1) nor vascular cell adhesion molecule 1 (VCAM-1), in the nasal mucosa was suppressed in the infliximab-treated group when compared to the nontreated group.
  
  
  CONCLUSIONS
  This study shows that the TNF-α inhibitor infliximab induces anti-allergic effects by decreasing local and systemic Th2 cytokine (IL-4) production, total and OVA-specific IgE levels, adhesion molecule (E-selectin) expression, and eosinophil infiltration into the nasal mucosa in an allergic rhinitis model. Therefore, infliximab should be considered as a potential agent in treating allergic rhinitis.
authors.affiliation: Department of Otorhinolaryngology, Dankook University, Cheonan, Chungcheongnam-do, Korea.
authors.forename: J-H
authors.initials: JH
authors.lastname: Mo
authors.forename: E-K
authors.initials: EK
authors.lastname: Kang
authors.forename: S-H
authors.initials: SH
authors.lastname: Quan
authors.forename: C-S
authors.initials: CS
authors.lastname: Rhee
authors.forename: C H
authors.initials: CH
authors.lastname: Lee
authors.forename: D-Y
authors.initials: DY
authors.lastname: Kim
mesh_terms: D000818:Animals; D018926:Anti-Allergic Agents / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000008:administration & dosage / Q000494:pharmacology* / Q000627:therapeutic use; D015815:Cell Adhesion Molecules / Q000187:drug effects; D016207:Cytokines / Q000096:biosynthesis / Q000187:drug effects; D004804:Eosinophils / Q000187:drug effects; D006967:Hypersensitivity / Q000188:drug therapy*; D007073:Immunoglobulin E / Q000187:drug effects; D000069285:Infliximab; D051379:Mice; D008807:Mice, Inbred BALB C; D009297:Nasal Mucosa / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology; D012220:Rhinitis / Q000188:drug therapy*; D018418:Th2 Cells / Q000276:immunology
chemical_list: D018926:Anti-Allergic Agents; D000911:Antibodies, Monoclonal; D015815:Cell Adhesion Molecules; D016207:Cytokines; D007073:Immunoglobulin E; D010047:Ovalbumin; D000069285:Infliximab