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The Journal of Immunology, 2000, 165: 4051-4061.
Copyright © 2000 by The American Association of Immunologists

Endogenous and Exogenous IL-6 Inhibit Aeroallergen-Induced Th2 Inflammation1

Jingming Wang*, Robert J. Homer{dagger}, Qingsheng Chen* and Jack A. Elias2,*

* Section of Pulmonary and Critical Care Medicine, Department of Internal Medicine, and {dagger} Department of Pathology, Yale University School of Medicine, New Haven, CT 06520; and Pathology and Laboratory Medicine Service, Veterans Administration-Connecticut Health Care System, West Haven, CT 06516

Chronic Th2-dominated inflammation and exaggerated IL-6 production are characteristic features of the asthmatic airway. To understand the processes that are responsible for the chronicity of this response and the role(s) of IL-6 in the regulation of airway Th2 inflammation, we compared the responses induced by OVA in sensitized wild-type mice, IL-6 deficient (-/-) mice, and transgenic mice in which IL-6 was overexpressed in the airway (CC10-IL-6 mice). When compared with wild-type mice, IL-6-/- mice manifest exaggerated inflammation and eosinophilia, increased levels of IL-4, IL-5, and IL-13 protein and mRNA, exaggerated levels of eotaxin, JE/monocyte chemoattractant protein-1, macrophage inflammatory protein-1{alpha} and -2, and mRNA, increased bronchoalveolar lavage (BAL) TGF-ß1, and exaggerated airway responses to aerosolized methacholine. In contrast, CC10-IL-6 mice, on both C57BL/6 and BALB/c backgrounds, manifest diminished inflammation and eosinophilia, decreased levels of IL-4, IL-5, and IL-13 protein and mRNA, and decreased levels of bronchoalveolar lavage TGF-ß1. IL-6 also decreased the expression of endothelial VCAM-1 and airway responsiveness to methacholine in these animals. These alterations in the IL-6-/- and CC10-IL-6 mice were not associated with significant decreases or increases in the levels of IFN-{gamma}, respectively. These studies demonstrate that endogenous and exogenous IL-6 inhibit aeroallergen-induced Th2 inflammation and that this inhibition is not mediated by regulatory effects of IFN-{gamma}. IL-6 may be an important anti-inflammatory, counterregulatory, and healing cytokine in the airway.




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