The Biocide Triclosan Drives the Inflammatory Responses in Epithelial Cells and Macrophages via ROS-Mediated Activation of ERK/NF-κB Signaling Pathways.

Abstract

Triclosan (TCS) is an antimicrobial agent that is commonly spread and detected in various environmental matrices and organisms, including human tissues and biological fluids. A sustained inflammatory response is an important initial event in various disease developments. TCS-induced inflammatory response and its fundamental molecular mechanisms remain largely unexplored. In this current study, the impact of TCS exposure on inflammatory activation was investigated in both noncancerous (BEAS-2B) and cancerous (A549) lung epithelial cells in addition to murine macrophages (J774). The results revealed that TCS treatment could significantly induce various pro-inflammatory mediators' expression that includes cytokines and chemokines, in all cell types compared to the corresponding vehicle-treated cells. Further, TCS-mediated inflammatory response is associated with reactive oxygen species (ROS)-mediated activation of extracellular-signal-regulated kinase (ERK)1/2 and nuclear factor-kappa B (NF-κB) p65 signaling pathways. Scavenging of TCS-induced ROS by N-acetylcysteine (NAC) could mitigate signaling pathways activation. As expected, inhibitors specific for ERK1/2 (PD98059) and NF-κB p65 (IMD0354) signaling pathways efficiently attenuated TCS-induced inflammatory response in BEAS-2B cells. Thus, ROS/ERK/NF-κB axis contributes to the TCS-induced inflammatory response. Further, animal studies are required for a better understanding of TCS-mediated inflammatory response in various organs, including the lungs.