Discipline: Biological Sciences
Subcategory: Cancer Research
Kayla A. Rice - Hinds Community College-Utica Campus
Co-Author(s): Victoria Williams and Dominique Thompson, Alcorn State University, MS Esther Iyanobor, Georgetown University, Washington, DC Gerri Wilson, Austin Puckett, Michelle Tucci, and Hamed Benghuzzi, University of Mississippi Medical Center, MS
We hypothesize that inhaled corticosteroids are widely used for the treatment of patients with inflammatory lung disorders including asthma, chronic obstructive pulmonary disease, and sarcoidosis. Corticosteroids effectively reduce the production of inflammatory mediators such as cytokines and chemokines. Although these molecules are also essential for host defense responses, there is little data on their effects on type II pneumocytes, which is the reason why we did this study on A549 cells. In this study A549 type II pneumocytes were grown on 24 well plates and challenged with low (5 µg/mL), medium (25 µg/mL), or high (50 µg/mL) doses of triamcinolone acetonide (TA) for 24, 48, and 72 hours. Cellular protein levels were not affected at 24 and 48 hours following treatment with TA when compared to control untreated cells. Cellular protein levels showed a significant reduction after 72 hours following treatment with all doses of TA when compared to control cells. There were no apparent changes in reduced intracellular glutathione content at any time point. A decrease in nitric oxide was seen by 24 hours and remained suppressed after 48 hours. Morphological assessment of the cells indicated an increase in the number of karyolitic cells by 48 hours in all TA treated cells when compared to control untreated cells. After 72 hours, an increase in the number of cells with features consistent with karyohexis was observed. There also appeared to be a dose-dependent increase in the number of pyknotic cells when compared with control untreated cells. The biological half-life of TA is 18-36 hours. Normally drug metabolism occurs via the cytochrome P450 family to metabolize the drug. It is of particular significance that the cell line A549 cells are cancerous, and this study suggest that TA can repress the growth of the A549 cancer cell. Overall, the data shows that increased concentrations of TA have adverse effects on type II pneumocytes, which is important information because an intact pulmonary surfactant system is necessary for normal respiratory function. Our data suggest that increasing doses of TA may increase the loss of the surfactant producing cells and further impair the respiratory function. Additional studies are needed to evaluate the effects of lower concentrations of TA on specific genes responsible for cell growth and survival.
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Funder Acknowledgement(s): I would like to thank Dr. Michelle Tucci, Gerri Wilson and Austin Puckett for mentoring and helping me while in the Anesthesiology lab. I also would like to thank Dr. Hamed Benghuzzi for his help. This work was funded by an Institutional Development Award (IDeA) from the NIGMS under grant number P20GM103476.
Faculty Advisor: Michelle Tucci, Hamed Benghuzzi, Gerri Wilson, Austin Puckett, Noel Gardner,, email@example.com
Role: I performed all experimentation and research under the instruction of Dr. Michelle Tucci and Dr. Hamed Benghuzzi.