Sulforaphane as a modulator of inflammation induced by airborne toxins 4674

Abstract Description The combustion of biomass, commonly used for heating and cooking in low- and middle-income countries, produces harmful byproducts that can lead to chronic inflammation and impair immune responses. Sulforaphane, a compound found in cruciferous vegetables, is known for its strong anti-inflammatory and antioxidant properties. This study aimed to investigate whether sulforaphane could mitigate the inflammatory effects of wood smoke and acrolein exposure. RAW 264.7 murine macrophages and A549 human lung epithelial cells were pre-treated with sulforaphane and exposed to soluble wood smoke particles and acrolein. Various molecular biology techniques were employed to evaluate the inflammatory and oxidative effects of biomass smoke and the potential of sulforaphane to counteract these effects. The activation of intracellular kinases (ERK1/2, JNK, and Akt) was also examined. Our results show that both wood smoke and acrolein triggered a robust inflammatory response, which was significantly reduced by sulforaphane pre-treatment. Exposure to biomass smoke and acrolein led to the upregulation of several genes, including COX-2, MCP-1, MIP-2/IL-8, HO-1, and Nrf-2. Additionally, sulforaphane was found to reduce inflammation induced by TLR agonists. However, at higher concentrations, sulforaphane exhibited cytotoxicity. Overall, our findings suggest that sulforaphane, at lower concentrations, can effectively attenuate the inflammatory responses induced by biomass smoke exposure. Funding Sources University of Richmond Topic Categories Innate Immune Responses and Host Defense: Cellular Mechanisms (INC)