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<p>Household air pollution caused by biomass burning is strongly linked to pulmonary diseases, primarily due to the emission of fine particulate matter (PM<sub>2.5</sub>). Pulmonary macrophages, located in the interstitial space and alveolar lumen, are vulnerable to PM<sub>2.5</sub> exposure and play a crucial role in the resulting inflammatory responses. This study investigates the impact of biofuel smoke-derived PM<sub>2.5</sub> (BPM<sub>2.5</sub>) on the activation of the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome in macrophages. Short-term exposure to PM<sub>2.5</sub>-rich biofuel smoke in rats induced significant pulmonary inflammation, characterized by increased numbers of neutrophils and macrophages in the bronchoalveolar lavage fluid, along with elevated expression of NLRP3 and transient receptor potential channel 6 (TRPC6) in lung tissues. In vitro, BPM<sub>2.5</sub> exposure upregulated the expression of NLRP3 inflammasome components and TRPC6 in macrophages. Notably, knockout of <i>Trpc6</i> reversed the BPM<sub>2.5</sub>-induced increase in NLRP3, ASC, and Caspase&#xa0;1 expression, decreased intracellular Ca<sup>2+</sup> concentration ([Ca<sup>2+</sup>]<sub>i</sub>), and suppressed the release of pro-inflammatory cytokines IL-1β and IL-18. These findings highlight that BPM<sub>2.5</sub> activates the NLRP3 inflammasome via the TRPC6/Ca<sup>2+</sup>/NLRP3 pathway, contributing to inflammation. This study provides new insights into the molecular mechanisms underlying PM<sub>2.5</sub>-induced pulmonary inflammation and suggests potential approaches for the prevention and treatment of PM<sub>2.5</sub>-related respiratory diseases.</p> Graphical abstract <p></p>

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PM2.5 from biofuel smoke induces inflammatory response through the TRPC6/Ca2+/NLRP3 signaling pathway

  • 期刊论文

  • 发表日期：

    2025年6月16日

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  • Yan Chen,
  • Na Zhan,
  • Jinhuang Xu,
  • Yupeng Huang,
  • Yuying Su,
  • Zhongqin Liu,
  • Haisheng Feng,
  • Wenxin Ji,
  • Jiahao Liang,
  • Shenting Zhao,
  • Jianhua Li

摘要

Household air pollution caused by biomass burning is strongly linked to pulmonary diseases, primarily due to the emission of fine particulate matter (PM2.5). Pulmonary macrophages, located in the interstitial space and alveolar lumen, are vulnerable to PM2.5 exposure and play a crucial role in the resulting inflammatory responses. This study investigates the impact of biofuel smoke-derived PM2.5 (BPM2.5) on the activation of the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome in macrophages. Short-term exposure to PM2.5-rich biofuel smoke in rats induced significant pulmonary inflammation, characterized by increased numbers of neutrophils and macrophages in the bronchoalveolar lavage fluid, along with elevated expression of NLRP3 and transient receptor potential channel 6 (TRPC6) in lung tissues. In vitro, BPM2.5 exposure upregulated the expression of NLRP3 inflammasome components and TRPC6 in macrophages. Notably, knockout of Trpc6 reversed the BPM2.5-induced increase in NLRP3, ASC, and Caspase 1 expression, decreased intracellular Ca2+ concentration ([Ca2+]i), and suppressed the release of pro-inflammatory cytokines IL-1β and IL-18. These findings highlight that BPM2.5 activates the NLRP3 inflammasome via the TRPC6/Ca2+/NLRP3 pathway, contributing to inflammation. This study provides new insights into the molecular mechanisms underlying PM2.5-induced pulmonary inflammation and suggests potential approaches for the prevention and treatment of PM2.5-related respiratory diseases.

Graphical abstract