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Updated: Jan 22, 2026
Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
NLRP3 inflammasome activation is associated with PM2.5 -induced cardiac functional and pathological injury in mice
Shuyin Duan1, Na Wang1, Li Huang2
1Department of Occupational and Environmental Health, College of Public Health, Zhengzhou University, Zhengzhou, China.
Abstract:
Growing evidences indicate that inflammation induced by PM2.5 exposure has been considered as a major driving force for the development of cardiovascular diseases. However, the mechanisms underlying PM2.5 -induced cardiac injury remain unclear. This study aims to investigate the role of NLRP3 inflammasome in PM2.5 -induced cardiac functional and pathological injury in mice. In this study, BALB/c mice were intratracheally instilled with PM2.5 suspension (4.0 mg/kg BW) for 5 days to set up a cardiac injury model, which was evaluated by electrocardiogram monitoring, HE and Masson staining. Then, the effects of PM2.5 on the expression of α-SMA, NLRP3, IL-1β, and IL-18 proteins and the activation of caspase-1 and IL-1β were investigated. The results showed that PM2.5 exposure induced characteristic abnormal ECG changes such as the abnormality of heart rhythm, tachycardia, and T-wave reduction. Inflammatory cell infiltration and fibrosis were observed in the heart tissues of PM2.5 -exposed mice. Meanwhile, PM2.5 exposure increased the expression of α-SMA. And, NLRP3 activation-associated proteins of NLRP3, IL-1β, IL-18, Cleaved caspase-1 p10, and Cleaved IL-1β were upregulated in heart tissue of PM2.5 -induced mice. In summary, PM2.5 exposure could induce cardiac functional and pathological injury, which may be associated with the activation of NLRP3 inflammasome.
Insights
Particulate matter (PM2.5) exposure causes cardiac injury through inflammation. This study reveals that PM2.5 activates the NLRP3 inflammasome, contributing to cardiovascular disease development.
Area of Science:
- Environmental Health
- Cardiovascular Research
- Immunology
Background:
- Particulate matter (PM2.5) exposure is linked to cardiovascular diseases.
- The precise mechanisms of PM2.5-induced cardiac injury are not fully understood.
- Inflammation plays a key role in PM2.5-related heart damage.
Purpose of the Study:
- To investigate the role of the NLRP3 inflammasome in PM2.5-induced cardiac functional and pathological injury in mice.
- To elucidate the molecular pathways involved in PM2.5 cardiotoxicity.
Main Methods:
- Mice were exposed to PM2.5 via intratracheal instillation.
- Cardiac function was assessed using electrocardiogram (ECG) monitoring.
- Cardiac pathology was evaluated through HE and Masson staining, and protein expression analysis (α-SMA, NLRP3, IL-1β, IL-18, caspase-1).
Main Results:
- PM2.5 exposure led to abnormal ECG readings, including arrhythmias and T-wave reduction.
- Histological analysis revealed inflammatory cell infiltration and cardiac fibrosis in exposed mice.
- PM2.5 increased α-SMA expression and upregulated NLRP3 inflammasome components (NLRP3, IL-1β, IL-18, caspase-1 activation).
Conclusions:
- PM2.5 exposure induces significant cardiac functional and pathological damage in mice.
- The activation of the NLRP3 inflammasome is implicated in the pathogenesis of PM2.5-induced cardiotoxicity.
- Targeting the NLRP3 inflammasome may offer a therapeutic strategy for mitigating PM2.5-related cardiovascular injury.
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