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Roles of Interleukin-13 and Interferon-γ in Lung Inflammation*

Gabriele Grünig, DVM, PhD; Jean G. Ford, MD, FCCP; Debra D. Donaldson, MD; Rajeev Venkayya, MD; Cliff McArthur, MS; Elisabeth Hansell, MS; Viswanath A. Kurup, PhD; Martha Warnock, MD; Donna Rennick, PhD
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*From the Department of Pathology (Dr. Grünig), Columbia University, New York, NY; the Harlem Lung Center (Dr. Ford), Columbia University, New York, NY; the Genetics Institute (Dr. Donaldson), Cambridge, MA; the Department of Pathology (Ms. Hansell and Dr. Warnock) and the Lung Biology Center (Dr. Venkayya), the Howard Hughes Research Institute (Mr. McArthur), University of California, San Francisco, CA; Veterans Affairs Medical Center (Dr. Kurup), University of Wisconsin, Milwaukee, WI; and the DNAX Research Institute (Dr. Rennick), Palo Alto, CA.

Correspondence to: Gabriele Grünig, PhD, St. Luke’s-Roosevelt Hospital Center, 432 W 58th St, Laboratory 504, New York, NY 10019



Chest. 2002;121(3_suppl):88S. doi:10.1378/chest.121.3_suppl.88S
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In human patients, asthma frequently is associated with mixed T helper (Th) cell responses. Th2 and Th1 cytokines (eg, interleukin [IL]-13 and interferon [IFN]-γ) can be detected in the lungs simultaneously. However, very little is known about critical mediators for the pathologic and physiologic changes that are induced by mixed T-cell responses in the lungs. Furthermore, IFN-γ has been reported to inhibit or promote Th2-induced lung injury.

To address this controversy, we examined an asthma model induced by mixed Th cell responses. IL-13 was a partial mediator of airway hyperreactivity and goblet cell hyperplasia, while effects on inflammation could not be detected. In contrast, IL-13 was critical for airway physiologic changes and inflammation in a Th2-induced asthma model that was examined in parallel, as has been reported before. In order to address whether the simultaneous presence of IL-13 and IFN-γ had altered the responses in the lungs of the mice that had mixed T-cell responses to the antigen, wild-type mice were given recombinant cytokines intranasally. IFN-γ inhibited IL-13-induced goblet cell hyperplasia as well as the accumulation of eosinophils and neutrophils in BAL fluid. At the same time, when compared to single cytokines IFN-γ and IL-13 potentiated peribronchial, perivascular, and alveolar inflammation, IL-6 levels, and the numbers of natural killer and antigen-presenting cells in the BAL fluid.

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