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Increased allergic airway responses in a murine model of intestinal anaphylaxis
Abstracts S163
RATIONALE: In order to address the underlying mechanistic basis for the clinical observation that patients with asthma can have pulmonary symptoms triggered by specific foods, we have developed a murine model of oral allergen-induced diarrhea and investigated allergic airway responses. METHODS: Balb/c mice were sensitized with OVA/alum and then subjected to intragastric (i.g.) saline or OVA challenges. After OVA challenged mice developed diarrhea, mice were intranasally challenged with saline or OVA. Airway inflammation [e.g. bronchoalveolar lavage (BAL) eosinophilia, mucus production] and airway hyperresponsiveness (AHR) was assessed before and 18h after intranasal (i.n.) challenge. RESULTS: Intragastrically OVA-challenged mice presented a mild increase in BAL eosinophilia, AHR and mucus production even in the absence of intranasal OVA challenges. Interestingly, a single i.n. challenge with OVA induced significantly more airway inflammation in i.g. OVAchallenged mice compared to i.g. saline-challenged mice. A kinetic analysis revealed that the observed amplification of lung inflammation is sustained for up to 11 days after the last i.g. OVA challenge. CONCLUSION: Mice subjected to a gastrointestinal allergic reaction showed increased susceptibility to develop an asthma-like phenotype following a single intranasal allergen challenge. Thus, the present model represents a great tool to study the mechanism linking gastrointestinal allergy and asthma. Funding: NIH R01 AI/HL53479-01
554
Increased Allergic Airway Responses in a Murine Model of Intestinal Anaphylaxis
E. B. Brandt, T. A. Scribner, L. M. Hassman, M. E. Rothenberg; Dept of Pediatrics; Div of Allergy and Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH.
SUNDAY
J ALLERGY CLIN IMMUNOL VOLUME 113, NUMBER 2
RATIONALE: In order to address the underlying mechanistic basis for the clinical observation that patients with asthma can have pulmonary symptoms triggered by specific foods, we have developed a murine model of oral allergen-induced diarrhea and investigated allergic airway responses. METHODS: Balb/c mice were sensitized with OVA/alum and then subjected to intragastric (i.g.) saline or OVA challenges. After OVA challenged mice developed diarrhea, mice were intranasally challenged with saline or OVA. Airway inflammation [e.g. bronchoalveolar lavage (BAL) eosinophilia, mucus production] and airway hyperresponsiveness (AHR) was assessed before and 18h after intranasal (i.n.) challenge. RESULTS: Intragastrically OVA-challenged mice presented a mild increase in BAL eosinophilia, AHR and mucus production even in the absence of intranasal OVA challenges. Interestingly, a single i.n. challenge with OVA induced significantly more airway inflammation in i.g. OVAchallenged mice compared to i.g. saline-challenged mice. A kinetic analysis revealed that the observed amplification of lung inflammation is sustained for up to 11 days after the last i.g. OVA challenge. CONCLUSION: Mice subjected to a gastrointestinal allergic reaction showed increased susceptibility to develop an asthma-like phenotype following a single intranasal allergen challenge. Thus, the present model represents a great tool to study the mechanism linking gastrointestinal allergy and asthma. Funding: NIH R01 AI/HL53479-01
554
Increased Allergic Airway Responses in a Murine Model of Intestinal Anaphylaxis
E. B. Brandt, T. A. Scribner, L. M. Hassman, M. E. Rothenberg; Dept of Pediatrics; Div of Allergy and Immunology, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH.
SUNDAY
J ALLERGY CLIN IMMUNOL VOLUME 113, NUMBER 2