Immunomodulatory Effects of Atrazine in Human A549 Lung Epithelial Cells 2310225

Abstract Introduction The endocrine system is objectively essential for immune functioning and formation. Agents such as Atrazine (ATR) disrupt the ability of the endocrine system to signal the immune system, resulting in an increased risk of autoimmunity, cancer, and neurodegenerative diseases. Atrazine is sprayed on corn cropping systems across the United States, which introduces small particles that can be absorbed into the alveolar sacs, damaging epithelial lung cells and possibly impacting gas exchange. This molecule has been known to inhibit cytokine production, such as IL-6, and cell proliferation. However, there remains a gap in current research as to which pathways ATR inhibits. Methods This research utilized the A549 cell line to evaluate cytotoxic effects post ATR exposure. Atrazine was prepared in DMSO and diluted with media to obtain concentrations of 0, 5, 10, 20, 50, and 100 µM. Cells were exposed for periods of 24, 48, and 72 hours. Following exposure, MTT assay was utilized to confirm treatment with ATR did not result in cell death but remained metabolically active before immunocytochemistry can occur. Results The cell viability (%) mean after 24 hours at 100 μg/mL was significantly lowered to ∼50% when compared to the control of 100%. After both 48 and 72 hours of exposure to 50 and 100 μg/mL of ATR, cells showed significantly less metabolic activity when compared to the control. 48 hours with means of ∼50% and ∼25% for the 50 and 100 μg/mL, respectively, and 72 hours with means of ∼40% and ∼45% of ATR, respectively. Atrazine, particularly at higher concentrations for longer durations, decreased the cells’ metabolic activity, meaning ATR affected cell function. Conclusion Overall, the results indicate that ATR has a statistically significant effect on A549 cells at multiple concentrations over 24-to-72-hour time frames. Further research will dive into specific cytokine signaling pathways, to understand the mechanisms involved in immunomodulation. Funding Source This research project was funded in part by the Judith Strong Scholars research fund. Topic Categories Innate Immune Responses and Host Defense: Cellular Mechanisms (INC)