Evaluation of Soluble Tumour Necrosis Factor Receptor in Response to Silica Containing Dust and Asbestos Fibres Exposure

Pneumoconiosis is a disease caused by chronic exposure to mineral dust such as coal mine dust, silica and asbestos. Current concepts in the pathogenesis of pneumoconiosis suggest that the alveolar macrophage plays a central role in the outcome of this disease. Upon stimulation with mineral dust the macrophages secrete a number of fibrogenic cytokines among them tumor necrosis factor a (TNFa) which is considered to play a key role in mineral dust induced pneumoconiosis (Dubois etal., 1989; Donaldson, 1992; Donaldson etal., 1992; Vanhee etal., 1995). Recently, naturally occurring inhibitors of TNFa activity have been identified showing high affinity binding to TNFa (Brockhaus et al., 1990). These inhibitors have been characterised as extracellular domains of the TNFa receptors types I and II, respectively. In response to inflammatory stimuli that cause enhanced TNFa levels, they are shed from the cell surface and appear as extracellular receptors in body fluids (Porteu and Nathan, 1990). Since such extracellular soluble receptors are suggested to intervene in the regulatory mechanism for modulation of excessive TNFa activity (van Zee et al., 1992; Spinas et al., 1992), enhanced serum TNF-receptor levels may reflect overexpression of TNFa in response to chronic exposure of mineral dust. In order to study the role of soluble TNF receptor as an individual factor in pneumoconiosis development we investigated serum levels of sTNFRII in groups exposed to silica containing dust or asbestos with normal chest radiographics and in groups of patients with silicosis and asbestosis.