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.