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This Article Full Text Full Text (PDF) All Versions of this Article: 290/1/L170    most recent 00212.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Medoff, B. D. Articles by Luster, A. D. Search for Related Content PubMed PubMed Citation Articles by Medoff, B. D. Articles by Luster, A. D.

Antibody-antigen interaction in the airway drives early granulocyte recruitment through BLT1

¹Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Charlestown; and ²Pulmonary and Critical Care Unit, and ³Department of Pathology, Massachusetts General Hospital, Boston, Massachusetts

Submitted 12 May 2005 ; accepted in final form 19 August 2005

Antibody-antigen interactions in the airway initiate inflammation in acute asthma exacerbations. This inflammatory response is characterized by the recruitment of granulocytes into the airways. In murine models of asthma, granulocyte recruitment into the lung contributes to the development of airway hyperresponsiveness (AHR), mucus production, and airway remodeling. Leukotriene B₄ is a mediator released following antigen challenge that has chemotactic activity for granulocytes, mediated through its receptor, BLT1. We investigated the role of BLT1 in granulocyte recruitment following antigen challenge. Wild-type mice and BLT1^–/– mice were sensitized and challenged with ovalbumin (OVA) to induce acute allergic airway inflammation. In addition, to explore the relevance to antibody-antigen interactions, we injected OVA bound to anti-OVA IgG₁ or anti-OVA IgE intratracheally into naïve wild-type and BLT1^–/– mice. Cell composition of the lungs, cytokine levels, histology, and AHR were determined. After sensitization and challenge with ovalbumin, there was significantly reduced neutrophil and eosinophil recruitment into the airways of BLT1^–/– mice compared with wild-type animals after one or two daily antigen challenges, but this difference was not seen after three or four daily antigen challenges. Mucus production and AHR were not affected. Intratracheal injection of OVA bound to IgG₁ or IgE induced neutrophil recruitment into the airways in wild-type mice but not in the BLT1^–/– mice. We conclude that BLT1 mediates early recruitment of granulocytes into the airway in response to antigen-antibody interactions in a murine model of acute asthma.

lung inflammation; asthma; lipid mediator

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