House Dust and Triclosan Activated MAP Kinase Pathways in Lung Epithelial Cells

Graduate #15
Discipline: Biological Sciences
Subcategory: Cell and Molecular Biology

Djene Keita - Texas Southern University
Co-Author(s): Hyun-Min Hwang, Texas Southern University, Houston TX

Pharmaceuticals and personal care products (PPCPs) containing antimicrobial agents such as triclosan (TCS) are extremely popular. TCS is a biocide applied mainly in oral and cosmetic products such as toothpaste, mouthwash, soaps, makeups, and deodorants. It is a lipophilic compound and as such, has the potential to bioaccumulate and persist in the body thereby causing detrimental health effects. Significant concentrations of TCS have been detected in human fluids like urine, serum and breast milk. Through widespread manufacturing and usage, the presence of TCS in the environment (water, air, sediment, biota and dust) has been steadily increasing thereby raising concerns regarding its potential association with various human health conditions. Our usage of aerosols and cleaning products along with direct leaching from plastic materials, textiles and carpets treated with TCS contribute to its presence in in-door dust. Previous studies found TCS levels in indoor dust ranging from 17ng/g to 2870ng/g. Humans, particularly toddlers, are exposed to dust from indoor atmospheres through inhalation and oral ingestion. The ubiquitous presence of TCS in house dust represents a source of chronic exposure and has been related to asthma and allergies. Not much is known about the toxicological and biological effects of TCS in the human body after long-term and low-concentration exposure.

We hypothesized that triclosan produces increased inflammatory responses by activating pro-inflammatory signaling pathways in lung cells. To test this, cell viability was initially assessed following treatments of TCS over a 72-hour time period. We additionally examined the effect of TCS on the c Jun N- terminal kinase (JNK) and P38 mitogen activated protein (MAP) kinase pathway in lung epithelial cell lines using western blot analysis. We investigated the effect of TCS on JNK pathway in A549 lung epithelial cells. Our results indicate that TCS activated the JNK and p38 pathway by phosphorylation of JNK in a time and dose dependent manner. Future research involves understanding the translocation of Nuclear Factor- Kappa B (Nf-κB) pathway from triclosan exposure.

ERN Final Abstract (2016).docx

Funder Acknowledgement(s): This project was supported by the National Science Foundation Research Infrastructure in Science and Engineering (HRD 1345173).

Faculty Advisor: Shishir Shishodia, shishodias@tsu.edu