Enhanced release of an alveolar macrophage-derived chemoattractant for fibroblasts in rats after asbestos inhalation.

Our studies indicate the effects of in vivo asbestos exposure on the ability of alveolar macrophages (AM) to elaborate a chemoattractant for fibroblast using a rat model of asbestos inhalation. Two groups of rats were exposed by intermittent inhalation (6 hr/day for 5 days/week over a total period of 4 weeks) to either amphibole (crocidolite) or serpentine (chrysotile) asbestos. A group of control rats were sham-exposed to clean air only.

The effects of asbestos inhalation on the distribution and enhancement of immunoassociated antigen expression of alveolar macrophage subpopulation.

We have studied the effects of in vivo asbestos exposure on the surface immune-associated (Ia) antigen expression and distribution of alveolar macrophage subpopulations defined by continuous iso-osmotic Percoll gradients (density range: 1.006 to 1.123 g/ml) using a rat model of asbestos inhalation.

Enhanced interleukin activity following asbestos inhalation.

Asbestos inhalation can cause pulmonary fibrosis and is associated with a variety of immunological abnormalities. The purpose of this study was to evaluate the effects of asbestos inhalation on interleukin-1 (IL-1) and interleukin-2 (IL-2) production in a rodent model. Two groups of rats were exposed, by intermittent inhalation, to either amphibole (crocidolite) or serpentine (chrysotile) asbestos.