Talc particles and pleural mesothelium interface modulate apoptosis and inflammation

Abstract

Talc pleurodesis is the most used method to prevent recurrence of malignant pleural effusion (MPE). Inflammatory response produced by pleural mesothelial (PMC) and neoplastic cells and its relationship to effectiveness of pleurodesis is discussed. Aim Determination of the role of PMC and neoplastic cells in initial phase and regulation of acute inflammatory response to talc. Methods PMC cultures from transudative effusion and Lewis lung cancer (LLC) cells were divided into 5 groups: 100% PMC, 100% LLC, 25% PMC + 75% LLC, 50% of each cell line, and 75% PMC + 25% LLC. All were exposed to talc for 48 hours and IL-6, TNFRI measured along with the percentage of apoptosis. Results The production of IL-6 and TNFRI was highest in the culture of 100% PMC, diminished proportionally with the reduction in the percentage of this cell type; the culture that contained only LLC had the lowest levels of these cytokines. The percentage of apoptosis was most evident in cultures of 100% LLC. Conclusions Contact of talc with the mesothelium is pivotal to the initiation of the inflammatory process with production of mediators that lead to pleural inflammation. Talc induces apoptosis in tumor cells promoting less aggressive action in mesothelial cells, thus contributing to better control of MPE.