Abstract
Different cytokines are involved in the immune response in a very manifold manner as became evident in the last few years. We report about cytokines from quartz dust exposed human mononuclear cells which may be important in the development of silicosis. In chronic experimental silicosis, pulmonary fibrosis is associated with an intense inflammatory response. The predominant cell in the interstitium and the airspaces is the macrophage. But neutrofils also accumulate in the silicotic lung, especially in the early phases. Mechanisms, by which inflammation is initiated and modulated in the lung exposed to silica are poorly understood. Therefore, we investigated the hypothesis, that nondirect cascade mechanisms of quartz toxicity may be involved in human lung tissue damage. Several reports indicate that monocytes / macrophages produce and release a number of mediators after contact with quartz dust in both human and animal systems (3). These mediators include interleukin — 1, which is a potent inflammatory cytokine (6). Granulocytes, appearing early in rat alveoli after inhalation of quartz dust DQ-12 (2), might contribute to quartz induced tissue damage. However, quartz dust DQ-12 has been reported not to be stimulatory for granulocytes by itself.
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