Poster ()- #SCSOT20 - KEYWORDS: IL17, APOPTOSIS, DIESEL PARTICULATE EXTRACT

DIESEL PARTICULATE EXPOSURE: CROSS-TALK BETWEEN IL-17 FAMILY AND APOPTOTIC PATHWAY GENES

N. Bidarimath, A. Abdulkadir, S. Batra
Laboratory of Pulmonary Immunotoxicology, Department of Environmental Toxicology, Southern University and A&M College, Baton Rouge, Louisiana-70813, USA

ABSTRACT:
DIESEL PARTICULATE EXPOSURE: CROSS-TALK BETWEEN IL-17 FAMILY AND APOPTOTIC PATHWAY GENES N. Bidarimath, A. Abdulkadir, S. Batra Laboratory of Pulmonary Immunotoxicology, Department of Environmental Toxicology, Southern University and A&M College, Baton Rouge, Louisiana-70813, USA Pulmonary health is routinely challenged with a variety of environmental factors, that directly influence the viability and function of the lungs. One of the environmental factors is the emission from heavy diesel engine motors being used in robust mass transportation, railroads, heavy-duty combustion engines in construction, farmland, and mining industrial settings. The emission from these sources contain harmful chemicals such as benzene, chrysene, formaldehyde, nitrous oxide, and several other organic and inorganic substances. Diesel particulate matter/extract (DPM/DPE) can cause immunomodulatory effects, including inflammatory oxidative stress and apoptosis. However, the molecular mechanisms associated with DPE-induced responses are still not clear. While, apoptosis (programmed cell death) is essential for normal homeostasis, maturation of the immune system, and cellular defense; earlier studies demonstrate IL-17 mediated regulation apoptosis in pathological conditions. The current study is aimed at investigating the role of IL-17 in proliferation, apoptosis, and inflammation using human alveolar epithelial cells (A549) with type II characteristics. In brief, A549 cells were treated with various concentrations of DPE (1 mM, 10 mM, and 25 mM) for 24 and 48 hours and the samples were processed to determine IL-17A, IL-17F and IL-17R transcriptional levels and the apoptotic genes. Our preliminary studies demonstrate significant increase in the transcription of IL-17A and IL-17R in DPE-challenged A549 cells. Interestingly, we also observed increased transcription of-IL-1β and TNF-α; proapoptotic genes-BAX, BAK, FADD, FAS; and executioner/effector caspase-8 and caspase-3 in DPE exposed A549 cells. Further studies are in progress to evaluate-a) DPE-induced translational changes in cytokine/chemokine levels and apoptotic markers; and b) the impact of IL-17A/IL-17F neutralization on apoptotic markers in DPE exposed A549 cells. Type of Presentation: Poster Consider for award: Graduate Student