The macrophage respiratory burst

The cytotoxic action of macrophages is due to production of radicals, including halogen, nitric oxide and oxygen radicals. This means that infection can lead to a considerable increase in the total radical burden in the body. As discussed in section 8.5.1, this may be an important factor in the protein—energy deficiency disease kwashiorkor.

Stimulation of macrophages leads to a considerable increase in the consumption of glucose (the respiratory burst), which is metabolized by the pentose phosphate pathway (section 5.4.2), leading to increased production of NADPH. The respiratory burst oxidase (NADPH oxidase) is a flavoprotein that transfers electrons from NADPH onto cytochrome b558, which then reduces oxygen to superoxide. The reaction is:

The respiratory burst oxidase is a transmembrane multienzyme complex that is activated in response to:

  • complement fragment C5a which arises from the antibody—antigen reaction;
  • peptides containing N-formyl-Met-Leu-Phe, which may be bacterial or arise from the mitochondria of damaged tissue;
  • cytokines and other signalling molecules released in response to infection, including platelet-activating factor, leukotrienes and interleukins.
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