Release of lnterleukin-1 and Tumor Necrosis Factor by Rat Alveolar Macrophages after In Vivo or In Vitro Exposure to Mineral Dusts

Abstract

An important role in the pathogenesis of chronic fibrotic lung diseases has been ascribed to the alveolar macrophage (AM). This cell, depending on its state of activation, has the capacity to regulate various immunologic and inflammatory responses through the elaboration of biologically active cytokines. Two major macrophage-derived cytokines are interleukin-1 (IL-1) and tumor necrosis factor (TNF). IL-1, has been suggested as an AM-derived factor that is active in fibrogenic responses to mineral dusts (Schmidt et al., 1984). Since TNF, like IL-1, has pro-inflammatory activities, and recent reports indicate it can modulate fibroblast growth (Vilcek et al., 1986), it too may play a role in the development of pulmonary inflammation and fibrosis following mineral dust exposure.