Production of Tumor Necrosis Factor-α and Interleukin-6 by Human Alveolar Macrophages Exposed In Vitro to Coal Mine Dust

Abstract

Following our previous demonstration of cytokine secretion by alveolar macrophages (AM) from coal miners and from patients with coal workers' pneumoconiosis, we investigated the effect of in vitro exposure to coal dust and to its silica content on tumor necrosis factor-alpha (TNF), interleukin (IL)-1 beta, and IL-6 production by normal human AM. TNF and IL-1 beta concentrations were estimated by a specific radioimmunoassay, while IL-6 levels were evaluated by the proliferation of 7TD1 cells. After 24-h culture, coal dust triggered a significant release of TNF and IL-6 at the dose of 0.1 mg/ml and more obviously at 1 mg/ml in comparison with titanium dioxide (TiO2), used as a biologically inert control dust (with 1 mg/ml of dust: 3,526 +/- 3,509 versus 330 +/- 138 pg TNF/ml and 224 +/- 74 versus 72 +/- 34 U IL-6/ml, respectively; P less than 0.01 in both cases). After 3-h culture, a significant TNF secretion as well as an increased TNF mRNA expression were also detected for AM stimulated by coal dust at variance with TiO2. In contrast, no modification of IL-1 beta concentration could be evidenced in AM exposed to coal dust, although we detected an increased expression of specific mRNA expression. In order to define the role of silica among the main components of coal dust in AM activation, we evaluated the effect of silica (alpha-quartz, 30 micrograms/ml, which is the concentration and the type of silica present in our coal dust) alone or mixed with TiO2 (1 mg/ml) on monokine production.(ABSTRACT TRUNCATED AT 250 WORDS)

Thiol regulation of the production of TNF-α, IL-6 and IL-8 by human alveolar macrophages

“…mL -1 . This quantity was insufficient to trigger TNF-a mRNA expression and secretion as previously demonstrated [19]. Cells were allowed to adhere to plastic Petri dishes (2 mL in a 35-mm diameter well) for 2 h at 378C.…”

“…AMs were isolated by adherence as previously described [19]. Briefly, the lavage fluid was filtered through sterile surgical gauze and centrifuged at 4006g for 10 min at 48C.…”

Particulate-Cell Interactions and Pulmonary Cytokine Expression

“…Our initial data suggest that not only do type II cells show increased abundance of cytokine mRNA (27), but acute and chronic pulmonary inflammation lead to alterations in epithelial marker gene expression. We believe changes in such marker genes, in the absence of specific morphological evidence of cytotoxicity and epithelial damage, indicate a change in the activation state of the epithelium and may act as a marker for Figure 6. Measurement of IL-1 release by primary isolated type 11 cells in culture.…”

Effects of mineral fibers on the expression of genes whose product may play a role in fiber pathogenesis.

“…In inflammatory reactions, IL-6 could act as not only a proinflammatory cytokine because of its ability to induce the expression of cellular adhesion molecules on monocytes and the facilitation of their infiltration into the lung, but also as an antiinflammatory cytokine that inhibits the production of TNF and IL-1 (21). An increase has been reported in IL-6 released by bronchoalveolar cells from rats treated with asbestos or coal mineral dust (22).…”