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Hub AI
Respiratory burst AI simulator
(@Respiratory burst_simulator)
Hub AI
Respiratory burst AI simulator
(@Respiratory burst_simulator)
Respiratory burst
Respiratory burst (or oxidative burst) is the rapid release of the reactive oxygen species (ROS), superoxide anion (O−
2) and hydrogen peroxide (H
2O
2), from different cell types.
This is usually utilised for mammalian immunological defence, but also plays a role in cell signalling. Respiratory burst is also implicated in the ovum of animals following fertilization. It may also occur in plant cells.
Immune cells can be divided into myeloid cells and lymphoid cells. Myeloid cells, including macrophages and neutrophils, are especially implicated in the respiratory burst. They are phagocytic, and the respiratory burst is vital for the subsequent degradation of internalised bacteria or other pathogens. This is an important aspect of the innate immunity.
Respiratory burst requires a 10 to 20 fold increase in oxygen consumption through NADPH oxidase (NOX2 in humans) activity. NADPH is the key substrate of NOX2, and bears reducing power. Glycogen breakdown is vital to produce NADPH. This occurs via the pentose phosphate pathway.
The NOX2 enzyme is bound in the phagolysosome membrane. Post bacterial phagocytosis, it is activated, producing superoxide via its redox centre, which transfers electrons from cytosolic NADPH to O2 in the phagosome.
2O2 + NADPH —> 2O2•– + NADP+ + H+
The superoxide can then spontaneously or enzymatically react with other molecules to give rise to other ROS. The phagocytic membrane reseals to limit exposure of the extracellular environment to the generated reactive free radicals.
There are 3 main pathways for the generation of reactive oxygen species or reactive nitrogen species (RNS) in effector cells:
Respiratory burst
Respiratory burst (or oxidative burst) is the rapid release of the reactive oxygen species (ROS), superoxide anion (O−
2) and hydrogen peroxide (H
2O
2), from different cell types.
This is usually utilised for mammalian immunological defence, but also plays a role in cell signalling. Respiratory burst is also implicated in the ovum of animals following fertilization. It may also occur in plant cells.
Immune cells can be divided into myeloid cells and lymphoid cells. Myeloid cells, including macrophages and neutrophils, are especially implicated in the respiratory burst. They are phagocytic, and the respiratory burst is vital for the subsequent degradation of internalised bacteria or other pathogens. This is an important aspect of the innate immunity.
Respiratory burst requires a 10 to 20 fold increase in oxygen consumption through NADPH oxidase (NOX2 in humans) activity. NADPH is the key substrate of NOX2, and bears reducing power. Glycogen breakdown is vital to produce NADPH. This occurs via the pentose phosphate pathway.
The NOX2 enzyme is bound in the phagolysosome membrane. Post bacterial phagocytosis, it is activated, producing superoxide via its redox centre, which transfers electrons from cytosolic NADPH to O2 in the phagosome.
2O2 + NADPH —> 2O2•– + NADP+ + H+
The superoxide can then spontaneously or enzymatically react with other molecules to give rise to other ROS. The phagocytic membrane reseals to limit exposure of the extracellular environment to the generated reactive free radicals.
There are 3 main pathways for the generation of reactive oxygen species or reactive nitrogen species (RNS) in effector cells: