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: Interactions in Lung Inflammation1
*
Department of Medicine, Harlem Hospital Center, Harlem Lung Center, Columbia University, New York, NY 10037;
DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304;
Genetics Institute, Cambridge, MA 02140;
Lung Biology Center and
¶ Howard Hughes Medical Institute, Departments of Medicine and
||
Pathology, University of California, San Francisco, CA 94143;
#
Veterans’ Affairs Medical Center and Allergy Immunology Division, Medical College of Wisconsin, Milwaukee, WI 53295; and
**
Department of Pathology, Columbia University of Physicians and Surgeons and St. Luke’s-Roosevelt Hospital, New York, NY 10019
Chronic inflammatory diseases of the lungs, such as asthma, are
frequently associated with mixed (Th2 and Th1) T cell responses. We
examined the impact of critical Th1 and Th2 cytokines, IFN-
and
IL-13, on the responses in the lungs. In a mouse model of airway
inflammation induced by mixed T cell responses, the number of Th1
(IFN--positive) cells was found to be negatively correlated with
airway hyperreactivity. In these mice, blockade of IL-13 partially
inhibited airway hyperreactivity and goblet cell hyperplasia but not
inflammation. In contrast, in mice that responded with a polarized Th2
response to the same Ag, blockade of IL-13 inhibited airway
hyperreactivity, goblet cell hyperplasia, and airway inflammation.
These results indicated that the presence of IFN- would modulate the
effects of IL-13 in the lungs. To test this hypothesis, wild-type mice
were given recombinant cytokines intranasally. IFN- inhibited
IL-13-induced goblet cell hyperplasia and airway eosinophilia. At the
same time, IFN- and IL-13 potentiated each other’s effects. In the
airways of mice given IL-13 and IFN-, levels of IL-6 were increased
as well as numbers of NK cells and of CD11c-positive cells expressing
MHC class II and high levels of CD86. In conclusion, IFN- has
double-sided effects (inhibiting some, potentiating others) on
IL-13-induced changes in the lungs. This may be the reason for the
ambiguous role of Th1 responses on Th2 response-induced lung
injury.
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