Abstract
Oxidative stress, particularly reactive oxygen species (ROS), are important for innate immunity against pathogens. ROS directly attack pathogens, regulate and amplify immune signals, induce autophagy and activate inflammation. In addition, production of ROS by pathogens affects the endoplasmic reticulum (ER) and mitochondria, leading to cell death. However, it is unclear how ROS regulate host defense mechanisms. This review outlines the role of ROS during intracellular pathogen infection, mechanisms of ROS production and regulation of host defense mechanisms by ROS. Finally, the interaction between microbial pathogen-induced ROS and the ER and mitochondria is described.
Highlights
reactive oxygen species (ROS) in MitochondriaROS are chemically reactive oxygen metabolites, produced as byproducts of aerobic metabolism in all living cells
Phagocytized pathogens are degraded in phagocytes, which is boosted by the socalled oxidative burst [1]
Rapidly occurring oxidative burst is involved in the generation of nitric oxide and reactive oxygen species (ROS) [1,3]
Summary
ROS are chemically reactive oxygen metabolites, produced as byproducts of aerobic metabolism in all living cells. I–IV) and two factors (cytochrome c, coenzyme Q10) in the mitochondrial intermembrane space [23] and mediates oxidative phosphorylation [24]. During ATP generation, electrons released from the mitochondrial ETC incompletely reduce O2 to superoxide [25]. Mn-SOD in the mitochondrial matrix or SOD in the intermembrane space convert superoxide into. 1–2% of O2 is incompletely reduced to superoxide [27], mainly in complexes I and III of the mitochondrial respiratory chain [26,28,29]. Complex I generates superoxide by NADH-linked forward electron transport and succinate-linked reverse electron transport [27,31]. Mitochondrial superoxide production is triggered by an increase in the NADH/NAD+ ratio in the matrix [32].
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