Susceptibility of Diabetics to Air Pollution: The Role of Activation of NLRP3 Inflammasome in Alveolar Macrophages Exposed to Ambient PM2.5 In A High Glucose Environment
JSHS · 2022
Overview
Epidemiological studies have shown that individuals with preexisting conditions, such as asthma, COPD, fatty liver disease, and diabetes mellitus (DM), are more susceptible to air pollution. However, the underlying mechanisms are still unclear. The effects of ambient fine particulate matter (PM2.5) on mouse alveolar macrophages MH-Sand the involvement of IL-1β in the increased susceptibility of macrophages to PM2.5 in a high glucose environment were investigated. The results showed that exposure of alveolar macrophages to non-cytotoxic doses of PM2.5 led to up-regulation of proinflammatory cytokine IL-1β, activation of NLRP3 inflammasome, increased nuclear translocation of transcription factor NFkB, and ROS generation, which were enhanced when the cells were in a high glucose environment. Although PM2.5 exposure also caused TLR2 up-regulation, combined treatment of PM2.5 and high glucose had no enhanced effects on TLR2. These results suggest that enhanced production of proinflammatory cytokine IL-1β in alveolar macrophages exposed to PM2.5 with high glucose may be through activation of NLRP3 inflammasome due to PM2.5-induced oxidative stress and increased NFkB nuclear translocation. This study not only provides further understanding of the potential mechanisms underlying the susceptibility of individuals with DM to air pollution, but also sheds light on potential preventative measures; diabetes medications that could prevent or reduce IL-1β production such as pioglitazone and glyburide may offer considerable therapeutic promise in high PM-polluted areas. In addition, to reduce PM2.5-induced oxidative stress, daily supplement of antioxidants such as vitamins Cand Eand fresh vegetable and fruits may be recommended for individuals with DM.
Competition history
- JSHS 2022
Resources
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