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The Journal of Immunology, 2002, 168: 5278-5286.
Copyright © 2002 by The American Association of Immunologists

IFN-{gamma}-Inducible Protein 10 (CXCL10) Contributes to Airway Hyperreactivity and Airway Inflammation in a Mouse Model of Asthma1

Benjamin D. Medoff2,*,{dagger}, Alain Sauty2,§, Andrew M. Tager*,{dagger}, James A. Maclean*, R. Neal Smith{ddagger}, Anuja Mathew*, Jennifer H. Dufour* and Andrew D. Luster3,*

* Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology, {dagger} Pulmonary and Critical Care Unit, and {ddagger} Department of Pathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114; and § Division of Allergology and Clinical Immunology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland

Allergic asthma is an inflammatory disease of the airways characterized by eosinophilic inflammation and airway hyper-reactivity. Cytokines and chemokines specific for Th2-type inflammation predominate in asthma and in animal models of this disease. The role of Th1-type inflammatory mediators in asthma remains controversial. IFN-{gamma}-inducible protein 10 (IP-10; CXCL10) is an IFN-{gamma}-inducible chemokine that preferentially attracts activated Th1 lymphocytes. IP-10 is up-regulated in the airways of asthmatics, but its function in asthma is unclear. To investigate the role of IP-10 in allergic airway disease, we examined the expression of IP-10 in a murine model of asthma and the effects of overexpression and deletion of IP-10 in this model using IP-10-transgenic and IP-10-deficient mice. Our experiments demonstrate that IP-10 is up-regulated in the lung after allergen challenge. Mice that overexpress IP-10 in the lung exhibited significantly increased airway hyperreactivity, eosinophilia, IL-4 levels, and CD8+ lymphocyte recruitment compared with wild-type controls. In addition, there was an increase in the percentage of IL-4-secreting T lymphocytes in the lungs of IP-10-transgenic mice. In contrast, mice deficient in IP-10 demonstrated the opposite results compared with wild-type controls, with a significant reduction in these measures of Th2-type allergic airway inflammation. Our results demonstrate that IP-10, a Th1-type chemokine, is up-regulated in allergic pulmonary inflammation and that this contributes to the airway hyperreactivity and Th2-type inflammation seen in this model of asthma.




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