Sulfur dioxide attenuates LPS-induced acute lung injury via enhancing polymorphonuclear neutrophil apoptosis

Sulfur dioxide reduces lipopolysaccharide-induced acute lung injury in rats

“…Inflammation is also important in the pathogenesis of lung injury caused by LPS [19]. In this study, MPO activity in the lung, a marker of tissue neutrophil infiltration, was clearly increased in the LPS groups.…”

“…Excessive and uncontrolled inflammatory responses within the lung as well as PAH can complicate the clinical course of ALI induced by endotoxin. Recent research indicates that SO 2 may be produced endogenously in vessels and lungs and regulates both vascular reactivity [21,25] and inflammatory responses [3,19,26]. SO 2 and its hydrated form, sulfite/bisulfite, are generated through the normal processing of sulfur-containing amino acids such as L-cysteine, and AAT can be a key enzyme in controlling the endogenous production of SO 2 .…”

“…Interactions between SO 2 and other gaseous mediators are potential mechanisms for the attenuation of PAH by SO 2 . For example, multiple studies have described the functional interaction between NO and SO 2 in spontaneous hypertension and atherosclerosis [18][19][20], implying that the presence of other gaseous molecules in the endothelium influences SO 2 availability and/or efficacy. In this study, we observed that LPS treatment precipitated endothelial injury ( Figs.…”

“…Endogenous SO 2 can be produced during the normal processing of sulfur-containing amino acids such as L-cysteine in vivo, which is first oxidized to L-cysteine sulfinate, and the latter can develop through transamination by aspartate aminotransferase into β-sulfinylpyruvate, which decomposes spontaneously to pyruvate and SO 2 , and it had been shown that the SO 2 /aspartate aminotransferase (AAT) pathway could regulate vascular activities and was involved in the inflammatory response in vascular and lung tissues [17,18]. In addition, our previous study suggested that SO 2 attenuates LPS-induced ALI via enhancing apoptosis of PMNs [19]. So, in this study, we decided to investigate and validate the hypothesis that endogenous gaseous SO 2 may also act as a messenger molecule that could regulate inflammatory responses and vascular reactivity of pulmonary arteries (PAs), which are particularly involved in ALI.…”

Ambient sulfur dioxide levels associated with reduced risk of initial outpatient visits for tuberculosis: A population based time series analysis

“…1 Recent studies found that endogenous SO 2 has a physiological role on the regulation of pulmonary and cardiovascular function at physiological concentrations. 6 A previous in vitro study suggested that exogenous SO 2 contributes to the inhibition of mycobacterium tuberculosis (M.tb) growth, which could be used to develop new medications to tackle multidrug resistant M.tb 7 . Tuberculosis (TB), an infection by M.tb, has been associated with the second largest mortality toll globally with an estimate of 9 million cases and 1.5 million deaths each year 8 .…”