ABSTRACT
Hypoxic stress of the gut may induce impairment of gut barrier function, ensuing translocation of gut-derived factors which can damage the function of remote organs, especially the development of acute lung injury (ALI). High altitude pulmonary edema (HAPE) is a non-cardiogenic pulmonary injury caused by hypoxia, while inflammation involved in the pathogenesis of HAPE has been gradually recognized. It has been also recognized that the cleavage and maturation of proinflammatory cytokines mediated by NLRP3 inflammasome play a crucial role in the pathogenesis of lung injury. Further investigation on the role of NLRP3 inflammasome in lung injury induced by gut hypoxic stress is of an important clinical significance for further improvement in the treatment of hypoxic inflammatory diseases.