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Myeloid-Specific SIRT6 Deletion Protects Against Particulate Matter (PM2.5)-Induced Airway Inflammation
Shaopeng Chen1,2, Mindan Wu3, Zhilin Xiong1
1Institute of Respiratory Diseases, The First Dongguan Affiliated Hospital of Guangdong Medical University, Dongguan, People's Republic of China.
Purpose:
Particulate matter (PM2.5) is a common risk factor for airway inflammation. Alveolar macrophages play a critical role in airway inflammation. Sirtuin 6 (SIRT6) is a class Ill histone deacetylase that exerts an anti-inflammatory effect in airway diseases. However, the role of SIRT6 on PM2.5-induced airway inflammation in macrophages remains unclear. We aimed to determine whether SIRT6 protects against PM2.5-induced airway inflammation in macrophages.
Methods:
The effect of SIRT6 on PM2.5-induced airway inflammation was assessed by using THP1 cells or bone marrow-derived macrophages (BMDMs) exposed to PM2.5 in vitro and myeloid cell-specific SIRT6 conditional knockout mice (Sirt6fl/fl-LysMCre) in vivo.
Results:
PM2.5 increased SIRT6 expression in THP1 cells, but SIRT6 gene silencing decreased PM2.5 induced inflammatory cytokines in THP1 cells. Moreover, the expression of SIRT6 and inflammatory cytokines was also decreased in BMDMs with myeloid-specific deletion of SIRT6 after stimulation of PM2.5. In vivo, Sirt6fl/fl-LysMCre mice substantially decreased airway inflammation in response to PM2.5 exposure.
Conclusion:
Our results revealed that SIRT6 promotes the PM2.5-induced airway inflammation in macrophages and indicated that inhibition of SIRT6 in macrophages may represent therapeutic strategy for airway disorders induced by airborne particulate pollution.
Insights
Sirtuin 6 (SIRT6) promotes airway inflammation caused by particulate matter (PM2.5). Inhibiting SIRT6 in macrophages could be a therapeutic strategy for pollution-induced airway disorders.
Area of Science:
- Environmental Health
- Immunology
- Molecular Biology
Background:
- Particulate matter (PM2.5) is a significant risk factor for airway inflammation.
- Alveolar macrophages are key players in the inflammatory response within the airways.
- Sirtuin 6 (SIRT6), a histone deacetylase, is known for its anti-inflammatory properties in airway diseases, but its specific role in PM2.5-induced inflammation in macrophages was unclear.
Purpose of the Study:
- To investigate the role of Sirtuin 6 (SIRT6) in macrophages during particulate matter (PM2.5)-induced airway inflammation.
- To determine if SIRT6 protects against or contributes to PM2.5-induced airway inflammation in macrophages.
Main Methods:
- In vitro studies utilized THP1 cells and bone marrow-derived macrophages (BMDMs) exposed to PM2.5.
- In vivo studies employed myeloid cell-specific SIRT6 conditional knockout mice (Sirt6-/-).
- Assessed the impact of PM2.5 exposure and SIRT6 manipulation on inflammatory markers.
Main Results:
- PM2.5 exposure increased SIRT6 expression in THP1 cells.
- SIRT6 gene silencing reduced PM2.5-induced inflammatory cytokines in THP1 cells.
- In knockout mice and BMDMs, reduced SIRT6 expression or deletion led to decreased airway inflammation following PM2.5 exposure.
Conclusions:
- SIRT6 promotes PM2.5-induced airway inflammation in macrophages.
- Targeting SIRT6 in macrophages may offer a therapeutic approach for airway diseases linked to airborne particulate pollution.
