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)
Tobacco smoke is a usual form of oxidant aggression present in the domestic environment. In the present study, the in vitro acute effects of a 2-cigarette smoke gas phase were evaluated on cell viability and cytokine secretion by alveolar macrophages (AM) from guinea pigs and human healthy subjects. Cell injury was estimated immediately after smoke exposure by evaluation of ATP cell content (measured by bioluminescence) and lactic dehydrogenase (LDH) release in the culture medium. LDH release was also measured when the interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF) activities were evaluated. No cytotoxic effect was found: The ATP cell content of both guinea pig AM and human AM did not significantly change after tobacco smoke exposure. Similarly, the LDH release in the culture medium was unchanged both immediately after tobacco smoke exposure and at the time of the cytokine evaluation (18-20 h later) compared to cells cultured in the air. The total protein synthesis by the guinea pig AM evaluated by 35S-L-methionine labeling was unaffected by tobacco smoke exposure. The production of IL-6 and TNF activities was evaluated 18-20 h after smoke exposure. The IL-6 activity was measured by the proliferation test of 7TD1 hybridoma cell line; the TNF activity was evaluated by the L929 mouse fibroblast cytotoxic test and by an immunoradiometric assay (for human AM). A 2-cigarette smoke exposure decreased both activities significantly. The exposure of the guinea pig AM reduced IL-6 activity by 24.3 +/- 6.7%, 42.4 +/- 7.8%, and 39.7 +/- 9.6% and TNF activity by 33.8 +/- 10.4%, 35.1 +/- 10.7%, and 38.8 +/- 9.9% (respectively unstimulated cells and AM activated by 0.1 and 10 micrograms LPS/mL). The decrease in monokine production by the human AM was, respectively, 57.8 +/- 8.8%, 59.7 +/- 11.4%, and 49.9 +/- 10.5% of IL-6 activity and 37.4 +/- 14.6%, 17.6 +/- 9.6%, and 37.2 +/- 6.3% of TNF activity. The possible release of cytokine inhibitors was also investigated. The inhibitory activity against recombinant TNF and IL-6 was evaluated in culture medium from unstimulated AM exposed to tobacco smoke and did not significantly differ from that of AM exposed to air, demonstrating that the decrease of monokine levels could not be explained by the release of inhibitory factors.(ABSTRACT TRUNCATED AT 400 WORDS)
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.