1 Introduction
Myeloperoxidase (MPO) is an important member of the haem peroxidase superfamily [1], which was found in primary azurophilic granules of neutrophils. In the presence of H2O2 and a halide—chloride, bromide, or thiocyanate, MPO can catalyzes the formation of reactive oxygen intermediates including hypochlorous (HOCl), and hypothiocyanous acids, respectively. Upon activation of neutrophils in peripheral blood and tissues, MPO is released into both the phagolysosomal compartment and the extracellular environment and then affects the aggregation of inflammatory cells under antigen stimulation [2,3]. Studies have shown that MPO not only plays a role in the process of killing pathogenic bacteria but also promotes the intensification of the inflammatory response and causes tissue damage [4]. MPO is part of the innate immune system that helps phagocytes fight against invading microorganisms and can significantly increase its activities in the pathological process of neurological diseases, tumours, rheumatoid diseases, kidney damage, diabetes and other diseases which participating in the initiation and progression of inflammation [5,6]. Recently, studies on MPO-mediated inflammatory events has become a hot topic. To define the in vivo role of MPO in host defense, MPO-knockout (MPO-/-) mice were created by two independent research groups and have been extensively studied for their susceptibility to infections. Mutant mice exhibit increased susceptibility to infection with C. albicans and Klebsiella pneumoniae compared to infected wild-type mice [7]. However, the role of MPO in regulating intestinal immune responses during infectious colitis and the mice response under hypoxia remains unclear. Here, we examined the inflammatory response of MPO-/- mice with intestinal bacterial infection merely, hypoxia merely, and bacterial infection accompanied with hypoxia than those in wild-type mice in order to explore the role of MPO in innate immunity.