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Review
. 2022 Apr;29(17):24445-24456.
doi: 10.1007/s11356-021-16405-w. Epub 2022 Jan 22.

PM2.5 exposure inducing ATP alteration links with NLRP3 inflammasome activation

Xiang Zeng  1 , Dongling Liu  2 , Weidong Wu  2 , Xia Huo  3
Affiliations
Review

PM2.5 exposure inducing ATP alteration links with NLRP3 inflammasome activation

Xiang Zeng et al. Environ Sci Pollut Res Int. 2022 Apr.

Erratum in

Abstract

Fine particulate matter (PM2.5) has been the primary air pollutant and the fourth leading risk factor for disease and death in the world. Exposure to PM2.5 is related to activation of the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, but the mechanism of PM2.5 affecting the NLRP3 inflammasome is still unclear. Previous studies have shown that PM2.5 can cause alterations in adenosine triphosphate (ATP), and an increase in extracellular ATP and a decrease in intracellular ATP can trigger the activation process of the NLRP3 inflammasome. Therefore, we emphasize that ATP changes may be the central link and key mechanism of PM2.5 exposure that activates the NLRP3 inflammasome. This review briefly elucidates and summarizes how PM2.5 acts on ATP and subsequently further impacts the NLRP3 inflammasome. Investigation of ATP changes due to exposure to PM2.5 may be essential to regulate NLRP3 inflammasome activation and treat inflammation-related diseases such as coronavirus disease 2019 (COVID-19).

Keywords: ATP; COVID-19; Energy metabolism; NLRP3 inflammasome; PM2.5.

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Conflict of interest statement

The authors declare no competing interests.

Figures

Fig. 1
Fig. 1
The mediation role of ATP alterations in the association between exposure to PM2.5 and activation of the NLRP3 inflammasome. Exposure to PM2.5 can induce ATP alterations. In addition, both PM2.5 exposure and ATP alteration can activate the NLRP3 inflammasome. Both exposure to PM2.5 and activation of NLRP3 inflammasome are related to COVID-19. Therefore, the review explores the mediation role of ATP alteration in the association of PM2.5 exposure, the NLRP3 inflammasome activation, and their related COVID-19
Fig. 2
Fig. 2
The potential ATP mediated pathway of PM2.5 exposure on NLRP3 inflammasome activation. Exposure to PM2.5 induce intracellular ATP decrease, which is linked with K+ efflux, Ca2+ influx, lysosome rupture, mitochondria disfunction, endoplasmic reticulum stress, and subsequently activate NLRP3 inflammasome
Fig. 3
Fig. 3
The process of ATP alteration activating the NLRP3 inflammasome. Both elevated extracellular ATP (ATP exposure) or decreased intracellular ATP (ATP efflux) can activate P2X7 receptor and open hemichannels such as pannexin-1 and connexin-43 in the cellular membrane, which result in various biological processes including mitochondria damage, lysosome rupture, and endoplasmic reticulum stress, and subsequently oxidative stress and inflammatory response, and finally activate the NLRP3 inflammasome
See this image and copyright information in PMC

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