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Am J Physiol Lung Cell Mol Physiol (September 22, 2006). doi:10.1152/ajplung.00503.2005
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Submitted on November 29, 2005
Accepted on July 6, 2006

Type-2 immune response associated with silicosis is not instrumental in the development of the disease

Pierre Misson1, Frank Brombacher2, Monique Delos3, Dominique Lison1, and Francois A Huaux1*

1 Unit of Industrial Toxicology and Occupational Medicine, Universite catholique de Louvain, Brussels, Belgium
2 Division of Immunology, IIDMM, Faculty of Health Science, University of Cape Town, Cap Town, South Africa
3 Laboratory of Pathology, University Hospital of Mont-Godinne, Yvoir, Belgium

* To whom correspondence should be addressed. E-mail: huaux{at}toxi.ucl.ac.be.

It has been proposed that the development of lung fibrosis is associated with a Th2 response, mainly characterized by IL-4 and IL-13 production. We investigated the potential role of type-2 immune polarization in the silicotic process and examined the pulmonary response to silica particles in mice genetically deficient for IL-4. We found that IL-4-/- mice were not protected against the development of silicosis, suggesting that IL-4 is not essential for the development of this fibrotic disease. By evaluating the intensity of silica-induced lung fibrosis in mice deficient for IL-4 receptor alpha (IL-4R{alpha}), we showed that the establishment of pulmonary fibrosis was independent of both IL-4 and IL-13. Strong impairment of the type-2 immune response (IgG1) in the lungs of IL-4-/- and IL-4R{alpha}-/- mice did not affect the development of the disease. Measurement of IL-13{alpha}2 receptor expression and IgG2a, IL-12p70 and IFN-{gamma} levels in silica-treated IL-4-/- and IL-4R{alpha}-/- animals showed that the development of silicosis was not related to an IL-13 signaling pathway or a switch to a type-1 response in deficient animals. Our data clearly indicate that the type-2 immune response associated with silicosis in mice is not required for the development of this inflammatory and fibrotic disease.




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