a; William W. Busse, MDb; Nizar N. Jarjour, MDa">
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Volume 111, Issue 1, Pages 79-86 (January 2003)


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A comparison of the airway response to segmental antigen bronchoprovocation in atopic asthma and allergic rhinitis☆☆

Elizabeth A. Becky Kelly, PhDa, William W. Busse, MDb, Nizar N. Jarjour, MDa

Received 14 June 2002; received in revised form 28 September 2003; accepted 4 October 2002.

Abstract 

Background: Patients with allergic asthma and those with allergic rhinitis (without asthma) share many immunopathologic features but differ in the presence of lower airway symptoms in response to antigen. Objectives: We sought to compare the airway inflammatory response to antigen in patients with atopic asthma and allergic rhinitis. Methods: Segmental bronchoprovocation with saline or ragweed antigen was performed in 9 patients with atopic asthma and 9 patients with allergic rhinitis without asthma. The antigen dose used in segmental bronchoprovocation was 10% of the dose that caused a 20% decrease in FEV1 in response to inhalation challenge. Bronchoalveolar lavage (BAL) was performed from the saline- and antigen-challenged segments at 5 minutes and 48 hours after challenge. BAL fluid was analyzed for cell count and differential, distribution of lymphocytes, and concentration of soluble factors (histamine, IL-5, matrix me-talloproteinase 9, tissue inhibitor of metalloproteinase 1, and fibronectin). In addition, BAL cells were cultured ex vivo, and IL-5, IFN-γ, and IL-10 generation was measured. Results: Antigen challenge led to similar patterns of cellular recruitment, mediator levels, and BAL cell cytokine generation in both groups; however, the dose of antigen required to promote comparable responses in the airway was significantly less in patients with asthma. Conclusion: These data suggest that the pattern of acute airway inflammation in response to allergen does not by itself explain antigen-induced lower airway obstruction and asthma symptoms. We speculate that other factors, such as increased airway sensitivity to allergen or preexisting airway injury and remodeling, might explain why patients with asthma and rhinitis differ in their clinical and physiologic response to antigen exposure. (J Allergy Clin Immunol 2003;111:79-86.)

Madison, Wis

From athe Pulmonary and Critical Care and bAllergy and Immunology Sections of the Department of Medicine, University of Wisconsin, Madison

 Supported by National Institutes of Health grant RO1 64066, an institutional Specialized Center of Research grant (NIH HL56396), and the American Lung Association of Wisconsin.

☆☆ Reprint requests: Elizabeth A. Becky Kelly, PhD, Section of Pulmonary and Critical Care Medicine, 600 Highland Ave, CSC K4/928, University of Wisconsin School of Medicine, Madison, WI 53792.

PII: S0091-6749(02)91290-X

doi:10.1067/mai.2003.28


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