Respiratory burst
Respiratory burst requires a 10 to 20 fold increase in oxygen consumption through NADPH oxidase (NOX2 in humans) activity.
Post bacterial phagocytosis, it is activated, producing superoxide via its redox centre, which transfers electrons from cytosolic NADPH to O2 in the phagosome.
The phagocytic membrane reseals to limit exposure of the extracellular environment to the generated reactive free radicals.
It may react directly with proteins that contain transition metal centers, such as FeS, releasing Fe2+ for the Fenton reaction.
Altered protein function includes changes in enzyme catalytic activity, cytoskeletal organisation and cell signal transduction.
[10] As many microbicidal products are formed during respiratory burst, the importance of individual molecules in killing invading pathogens is not wholly understood.
Due to the high toxicity of generated antimicrobial products including ROS, neutrophils have a short life span to limit host tissue damage during inflammation.
[12] Antioxidant enzymes counterbalance redox signalling by eliminating the involved molecules, importantly superoxide anion and nitric oxide.
The NADPH oxidase isoform NOX1 transiently produces a burst of superoxide in response to growth factor (e.g. EGF) stimulation of respective receptors.
Instead, their transient oxidative burst regulates the inflammatory response by inducing cytokine synthesis for redox signalling, resulting in an influx of neutrophils and activated macrophages.
In humans, mitochondrial ROS is required alongside those released in the oxidative burst for mitogenic pathway stimulation in oncogenic KRAS cells.
However, in oncogenic Kras mice fibroblasts, NADPH oxidase inhibitors have been shown to be sufficient to block these growth factor pathways.
However, the generated reactive species are maintained at lower levels than in immunity to protect the fertilised egg itself from oxidative damage.
This is achieved by the elimination of hydrogen peroxide primarily through the dual function of the same egg oxidase, and secondarily through cytoplasmic ROS scavengers, such as catalase and glutathione.
In plant immunity, the NADPH oxidase subunits RbohD and RbohF have overlapping functions are expressed in different tissues and at different levels.
[28] Systemic acquired resistance, which is analogous to innate immunity in animals, is also induced in the exposed plant cells.
