Experimental gastrointestinal allergy enhances pulmonary responses to specific and unrelated allergens - 16/08/11
Reprint requests: Marc E. Rothenberg, MD, PhD, Division of Allergy and Immunology, Department of Pediatrics, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229.Cincinnati, Ohio
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.
Conclusion |
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.
Clinical implications |
Experimental gastrointestinal allergy primes for responses to allergens in the respiratory tract, enhancing antigen-specific antibody and TH2 cytokine production, airway inflammation, and airway hyperresponsiveness.
Le texte complet de cet article est disponible en PDF.Key words : Allergy, lung, intestine, eosinophil, eotaxin, IL-13, house dust mite, ovalbumin, mice
Abbreviations used : Alum, BALF, HDM, OVA, PAS, Penh
Plan
| Supported in part by National Institutes of Health grants R01 AI42242, HL-076383, and AI057803 (M.E.R.). Disclosure of potential conflict of interest: M.E. Rothenberg has consultant arrangements with MEDACorp, GlaxoSmithKline, and Ception Therapeutics; owns stock in Ception Therapeutics; has received grant support from Cambridge Antibody Technology; and is on the speakers’ bureau for Merck. T.A. Scribner has received grant support from Adams Respiratory Therapeutics, Advance Life Sciences, GlaxoSmithKline, Genentech, Mylan-Bertek, MedPointe Pharma, and Oscient Pharmaceuticals; is employed by Baz Allergy, Asthma and Sinus Center; and is on the speakers’ bureau for GlaxoSmithKline and Sanofi-Aventis. The rest of the authors have declared that they have no conflict of interest. |
Vol 118 - N° 2
P. 420-427 - août 2006 Retour au numéro
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