The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/3/1089/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 6, March 17, 1997 1089-1100

Articles

Interleukin-10 Is a Natural Suppressor of Cytokine Production and Inflammation in a Murine Model of Allergic Bronchopulmonary Aspergillosis

Gabriele Grünig*, David B. Corry{ddagger}, Michael W. Leach§, Brian W.P. Seymour*, Viswanath P. Kurup||, and Donna M. Rennick*

From the * Department of Immunology, DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, California 94304; {ddagger} Department of Medicine, University of California, San Francisco, California 94110; § Schering-Plough Research Institute, Lafayette, New Jersey 07848; and the || Department of Medicine, Allergy Immunology Division, Medical College of Wisconsin and Research Service, Veterans' Administration Medical Center, Milwaukee, Wisconsin 53295

We have used interleukin-10 (IL-10) gene knockout mice (IL-10–/–) to examine the role of endogenous IL-10 in allergic lung responses to Aspergillus fumigatus Ag. In vitro restimulated lung cells from sensitized IL-10–/– mice produced exaggerated amounts of IL-4, IL-5, and interferon-{gamma} (IFN-{gamma}) compared with wild-type (WT) lung cells. In vivo, the significance of IL-10 in regulating responses to repeated A. fumigatus inhalation was strikingly revealed in IL-10–/– outbred mice that had a 50–60% mortality rate, while mortality was rare in similarly treated WT mice. Furthermore, IL-10–/– outbred mice exhibited exaggerated airway inflammation and heightened levels of IL-5 and IFN-{gamma} in bronchoalveolar lavage (BAL) fluids. In contrast, the magnitude of the allergic lung response was similar in intranasally (i.n.) sensitized IL-10–/– and wild-type mice from a different strain (C57BL/6). Using a different route of priming (intraperitoneal) followed by one i.n. challenge we found that IL-10–/– C57BL/6 mice had heightened eosinophilic airway inflammation, BAL–IL-5 levels, and numbers of {alpha}βT cells in the lung tissues compared with WT mice. We conclude that IL-10 can suppress inflammatory Th2-like lung responses as well as Th1-like responses given the constraints of genetic background and route of priming.

Address correspondence to Gabriele Grünig, D.V.M., Ph.D., DNAX Research Institute of Molecular and Cellular Biology, 901 California Avenue, Palo Alto, CA 94304.

DNAX Research Institute of Molecular and Cellular Biology is supported by Schering-Plough Corporation. This work was partially supported by a US Veterans Affairs Medical research grant (V.P. Kurup) and by grant HL 03344 from the National Institutes of Health (D.B. Corry).

1 Abbreviations used in this paper: ABPA, allergic bronchopulmonary aspergillosis; ACh, Acetylcholine; BAL, bronchoalveolar lavage; IL-10–/– mice, IL-10 gene knockout mice; i.n., intranasal; PC200, provocative challenge dose 200; WT mice, wild-type mice.


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