Advisor

Dr. Sanjay Batra

Second Advisor

2024

Document Type

Presentation

Abstract

Diesel particulate matter (DPM) is a form of human-made air pollution generated during the combustion process of heavy-duty diesel engines in various industrial sectors like agriculture, construction, maritime, and mining. Exposure to diesel particulate extract (DPE) in the workplace has been linked to inflammation and various lung diseases. Recent research has indicated that a reversible chemical modification process called SUMOylation, induced by SUMO-1, may play a crucial role in activating the inflammasome and causing programmed cell death (apoptosis)/Pyroptosis. However, the precise connection between DPE-induced SUMOylation and the activation of the inflammasome, apoptosis/pyroptosis remains unclear. To explore this further, experiments were conducted on human alveolar epithelial cells (A549), which exhibit characteristics like alveolar type II cells. Notably, exposure to DPE increased the mRNA levels of SUMO conjugating proteins (SUMO1, SUMO2/3), components of the NLRP3 inflammasome (NLRP3, ASC, CASP1), and pro-apoptotic genes, including initiator caspases (CASP8, CASP9) and executioner caspases (CASP3), in A549 cells. Interestingly, when SUMO1 was silenced using siRNA in DPE-exposed A549 cells, the expression of NLRP3, CASP1, and CASP3 was restored, suggesting that SUMO1 may play a role in activating NLRP3 and CASP3. Additionally, the release of inflammasomes into the extracellular space was detected upon cell death. Further investigations using both in vitro and in silico methods are currently ongoing to gain a more comprehensive understanding of these molecular mechanisms.

Presentation Date

3-27-2024

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