Discipline: Ecology Environmental and Earth Sciences
Subcategory: Cell and Molecular Biology
Djene Keita - Texas Southern University
Triclosan (2,4,4′-trichloro-2′-hydroxy-diphenyl ether) (TCS), is a widely used antimicrobial agent. Due to its antibacterial properties, triclosan is added in personal care products, hair products, household items, sports equipment as well as textiles and furniture, and many more. There is great potential that humans may be exposed to triclosan through oral and via contact with the lungs with constant exposure or usage of products containing this compound. There is concern about the bioaccumulation of triclosan. Pharmacokinetic studies in humans have indicated that triclosan can be absorbed from the gastrointestinal tract and skin. The presence of triclosan has been determined in human body fluids and tissues, including plasma, breast milk, urine, brain and liver tissues as well as hair and nails. The present study aimed to determine how triclosan, a ubiquitous compound, regulates mitogen-activated protein kinases (MAPKs) activity. The findings of this study will offer a significant contribution to the mechanism of action on the effects of triclosan exposure in the lungs when inhaled or in the gut when ingested, which may have deleterious effects. A549 and Beas-2B lung cells and HT-29 colon cells were used to study MAPK pathway. The cells were cultured, and viability determined by MTT and Live-Dead fluorescence assay. Expression and phosphorylation of extracellular signal-regulated protein kinases (ERKs), c-Jun amino-terminal kinase (JNK) and p38 MAPK, were investigated using Western immunoblot analysis. Nuclear translocation of nuclear factor-κB (NF-κB) p65 subunit was also examined using Western immunoblot analysis. Cytokines were measured by ELISA, and oxidative stress evaluated by microscopy. Activation of JNK, ERK, and p38 pathways by triclosan was cell type-specific. Triclosan activated JNK pathway in both lung cell types through different mechanisms. Triclosan induced phosphorylation of JNK through MKK7 in Beas-2B cells. However, activation of MKK4, not MKK7, promoted phosphorylation of JNK in A549 cells. In HT-29 colon cells, triclosan suppressed the phosphorylation of JNK. Triclosan also induced the expression of NF-κB in all cells in a time-dependent manner. Furthermore, triclosan affected the production of proinflammatory cytokines and reactive oxygen species (ROS) in all cell lines. Triclosan could potentially affect inflammation in the cells by affecting the production of proinflammatory cytokines which are mediated through activation of MAPK and NF-κB signaling pathways. Future research involves determining gene expression by measuring mRNA levels in response to triclosan.
Funder Acknowledgement(s): This research was primarily supported by the National Science Foundation (NSF) through Texas Southern University (TSU) under the award numbers HRD-1622993, BCS-1831205, and HRD-1829184.
Faculty Advisor: Shishir Shishodia, Shishir.Shishodia@tsu.edu
Role: I performed this entire research.