respiratory burst

During phagocytosis the phagocytic cell undergoes an increase in glucose and oxygen consumption termed the respiratory burst. The respiratory burst generates several oxygen-containing compounds that kill the bacteria uncergoing phagocytosis – oxygen-dependent intracellular killing. Bacteria can also be killed by pre-formed substances released from granules or lysosomes upon bacterial fusion with the phagosome – oxygen-independent intracellular killing.

1. Oxygen-dependent myeloperoxidase-independent intracellular killing.
During phagocytosis, glucose is metabolized via the pentose monophosphate shunt, with formation of NADPH. Cytochrome B from the granulocyte-specific granule combines with and activates plasma membrane NADPH oxidase. The activated NADPH oxidase then employs oxygen to oxidize the formed NADPH with resultant production of superoxide anion. A portion of the superoxide anion is converted to H2O2 plus singlet oxygen by superoxide dismutase. Additionally, superoxide anion can react with H2O2, resulting in the formation of hydroxyl radical plus more singlet oxygen. Together these reactions produce the toxic oxygen compounds superoxide anion (O2-), H2O2, singlet oxygen (1O2) and hydroxyl radical (OH•).

2. Oxygen-dependent myeloperoxidase-dependent intracellular killing
Fusion of azurophilic granules with the phagosome causes release of myeloperoxidase into the phagolysosome. Myeloperoxidase utilizes H2O2 and halide ions (usually Cl-) to produce highly toxic hypochlorite. Some hypochlorite spontaneously breaks down to yield singlet oxygen. Together these reactions produce toxic hypochlorite (OCl-) and singlet oxygen (1O2).

3. Detoxification reactions

Neutrophils and macrophages are able to protect themselves by detoxifying the toxic oxygen intermediates that they generate. Granulocyte self-protection is achieved in reactions employing the dismutation of superoxide anion to hydrogen peroxide by superoxide dismutase and the conversion of hydrogen peroxide to water by catalase.