Abstract
BackgroundLocal pulmonary and systemic infections can lead to acute lung injury (ALI). The resulting lung damage can evoke lung failure and multiple organ dysfunction associated with increased mortality. Hydrogen sulfide (H2S) appears to represent a new therapeutic approach to ALI. The gas has been shown to mediate potent anti-inflammatory and organ protective effects in vivo. This study was designed to define its potentially protective role in sepsis-induced lung injury.MethodsC57BL/6 N mice received lipopolysaccharide (LPS) intranasally in the absence or presence of 80 parts per million H2S. After 6 h, acute lung injury was determined by comparative histology. Bronchoalveolar lavage (BAL) fluid was analyzed for total protein content and differential cell counting. BAL and serum were further analyzed for interleukin-1β, macrophage inflammatory protein-2, and/or myeloperoxidase glycoprotein levels by enzyme-linked immunosorbent assays. Differences between groups were analyzed by one way analysis of variance.ResultsHistological analysis revealed that LPS instillation led to increased alveolar wall thickening, cellular infiltration, and to an elevated ALI score. In the presence of H2S these changes were not observed despite LPS treatment. Moreover, neutrophil influx, and pro-inflammatory cytokine release were enhanced in BAL fluid of LPS-treated mice, but comparable to control levels in H2S treated mice. In addition, myeloperoxidase levels were increased in serum after LPS challenge and this was prevented by H2S inhalation.ConclusionInhalation of hydrogen sulfide protects against LPS-induced acute lung injury by attenuating pro-inflammatory responses.
Highlights
Local pulmonary and systemic infections can lead to acute lung injury (ALI)
Acute lung injury (ALI), and the acute respiratory distress syndrome (ARDS), are two major challenges in clinical practice and both are responsible for high rates of morbidity and mortality amongst intensive care patients [1,2,3]
The underlying strong inflammatory response in sepsis-induced ALI is characterized by the transmigration of immune-competent cells
Summary
Local pulmonary and systemic infections can lead to acute lung injury (ALI). The resulting lung damage can evoke lung failure and multiple organ dysfunction associated with increased mortality. The underlying strong inflammatory response in sepsis-induced ALI is characterized by the transmigration of immune-competent cells (mostly neutrophils). In this respect, hydrogen sulfide (H2S) has come to be a focus of interest. H2S belongs to the group of gaseous transmitters, along with nitric oxide and carbon monoxide It is present in the blood and organs of humans and mammals in low micromolar extracellular concentrations. Exogenous application of gaseous H2S and H2S donors in different animal disease models like ventilator-induced lung injury [7], ischemia/reperfusion injury [8], or oleic acid-induced ALI [9,10], succeeded in exerting organprotective effects. The underlying mechanism may be explained by the ability of H2S to inhibit the activation and transmigration of neutrophil cells and to attenuate the release of pro-inflammatory cytokines
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