title: Experimental gastrointestinal allergy enhances pulmonary responses to specific and unrelated allergens.
abstract: BACKGROUND
  Gastrointestinal allergy often precedes or coexists with respiratory allergy.
  
  
  OBJECTIVE
  We hypothesized that established experimental gastrointestinal allergy would prime for the development of allergic respiratory responses.
  
  
  METHODS
  BALB/c mice were sensitized with ovalbumin (OVA) in the presence of aluminum potassium sulfate and then subjected to intragastric saline or OVA challenges. After the development of allergen-induced gastrointestinal allergy, mice were intranasally exposed to either saline, OVA, or a neoaeroallergen house dust mite (HDM) extract. Airway inflammation (eg, bronchoalveolar lavage fluid cellularity, cytokine levels, and OVA-specific antibody levels) and airway responsiveness to methacholine exposure were assessed after intranasal allergen exposure.
  
  
  RESULTS
  A single intranasal exposure to OVA induced significantly more airway inflammation in intragastric OVA-challenged mice compared with that seen in intragastric saline-treated mice. Kinetic analysis revealed that the observed amplification of lung inflammation was sustained for up to 12 days after the last intragastric OVA challenge after resolution of blood eosinophilia. When mice with gastrointestinal allergy were repeatedly challenged with HDM in the respiratory tract, they experienced enhanced airway inflammation, including bronchoalveolar lavage fluid eosinophilia and increased IL-13 levels.
  
  
  CONCLUSIONS
  Taken together, our results demonstrate that OVA-induced gastrointestinal allergy enhances not only allergic airway responses to OVA but also to HDM, an unrelated aeroallergen.
  
  
  CONCLUSIONS
  Experimental gastrointestinal allergy primes for responses to allergens in the respiratory tract, enhancing antigen-specific antibody and T(H)2 cytokine production, airway inflammation, and airway hyperresponsiveness.
authors.affiliation: Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.
authors.forename: Eric B
authors.initials: EB
authors.lastname: Brandt
authors.forename: Troy A
authors.initials: TA
authors.lastname: Scribner
authors.forename: Hiroko Saito
authors.initials: HS
authors.lastname: Akei
authors.forename: Marc E
authors.initials: ME
authors.lastname: Rothenberg
mesh_terms: D000485:Allergens / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D039741:Antigens, Dermatophagoides / Q000008:administration & dosage / Q000494:pharmacology*; D001249:Asthma / Q000139:chemically induced / Q000276:immunology; D016535:Bronchial Hyperreactivity / Q000139:chemically induced / Q000276:immunology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D004802:Eosinophilia / Q000139:chemically induced; D005260:Female; D005512:Food Hypersensitivity / Q000097:blood / Q000150:complications* / Q000276:immunology; D007070:Immunoglobulin A / Q000276:immunology; D007073:Immunoglobulin E / Q000032:analysis / Q000097:blood; D007074:Immunoglobulin G / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000008:administration & dosage / Q000494:pharmacology*; D011014:Pneumonia / Q000139:chemically induced / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000097:blood / Q000139:chemically induced / Q000209:etiology* / Q000276:immunology
chemical_list: D000485:Allergens; D039741:Antigens, Dermatophagoides; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007073:Immunoglobulin E; D010047:Ovalbumin