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Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis
Hui-Jie Ma1, Xin-Li Huang, Yan Liu
1Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China.
Aim:
We speculated that the enhanced apoptosis of polymorphonuclear neutrophil (PMN) might be responsible for the inhibition of PMN infiltration in the lung. This study was designed to investigate the effects of sulfur dioxide (SO(2)) on PMN apoptosis in vivo and in vitro, which may mediate the protective action of SO(2) on pulmonary diseases.
Methods:
Acute lung injury (ALI) was induced by intratracheally instillation of lipopolysaccharide (LPS, 100 μg/100 g, in 200 μL saline) in adult male SD rats. SO(2) solution (25 μmol/kg) was administered intraperitoneally 30 min before LPS treatment. The rats were killed 6 h after LPS treatment. Lung tissues were collected for histopathologic study and SO(2) concentration assay. Bronchoalveolar lavage fluid (BALF) was collected for the measurement of PMN apoptosis. For in vitro experiments, rat peripheral blood PMNs were cultured and treated with LPS (30 mg/L) and SO(2) (10, 20 and 30 μmol/L) for 6 h, and apoptosis-related protein expression was detected by Western blotting, and apoptosis rate was measured with flow cytometry.
Results:
LPS treatment significantly reduced the SO(2) concentrations in the lung tissue and peripheral blood, as compared with the control group. Pretreatment with SO(2) prevented LPS-induced reduction of the SO(2) concentration in the lung tissue and peripheral blood. LPS treatment significantly reduced PMN apoptosis both in vivo and in vitro, which could be prevented by the pretreatment with SO(2). The protein levels of Caspase-3 and Bax was significantly increased, but Bcl-2 was decreased by the pretreatment with SO(2), as compared with LPS administration alone.
Conclusion:
SO(2) plays an important role as the modulator of PMN apoptosis during LPS-induced ALI, which might be one of the mechanisms underlying the protective action of SO(2) on pulmonary diseases.
Insights
Sulfur dioxide (SO(2)) enhances polymorphonuclear neutrophil (PMN) apoptosis, counteracting lipopolysaccharide-induced lung injury. This modulation of PMN apoptosis may explain SO(2)
Area of Science:
- Pulmonary Medicine
- Toxicology
- Cell Biology
Background:
- Acute lung injury (ALI) involves polymorphonuclear neutrophil (PMN) infiltration.
- The role of sulfur dioxide (SO(2)) in modulating PMN apoptosis in ALI is not fully understood.
Purpose of the Study:
- To investigate the in vivo and in vitro effects of SO(2) on PMN apoptosis.
- To determine if SO(2)'s modulation of PMN apoptosis mediates its protective effects in pulmonary diseases.
Main Methods:
- Acute lung injury induced in rats via lipopolysaccharide (LPS) instillation.
- SO(2) administered intraperitoneally prior to LPS challenge.
- PMN apoptosis measured in bronchoalveolar lavage fluid and in vitro cultured PMNs.
- Western blotting used to detect apoptosis-related protein expression (Caspase-3, Bax, Bcl-2).
Main Results:
- LPS treatment reduced SO(2) concentrations and inhibited PMN apoptosis.
- SO(2) pretreatment prevented the reduction in SO(2) levels and restored PMN apoptosis.
- SO(2) increased pro-apoptotic proteins (Caspase-3, Bax) and decreased anti-apoptotic protein (Bcl-2).
Conclusions:
- SO(2) acts as a modulator of PMN apoptosis in LPS-induced ALI.
- Enhanced PMN apoptosis by SO(2) is a potential mechanism for its protective effects in pulmonary diseases.
