Learning Objective
Explain the steps, enzymes, ROS products, and clinical relevance of the respiratory burst in phagocytes — including the role of NADPH oxidase and the consequences of its deficiency (Chronic Granulomatous Disease).
The respiratory burst is a rapid, oxygen-dependent process used by neutrophils and monocytes/macrophages to kill pathogens. It is triggered after a pathogen is engulfed into a phagolysosome.
Activity
1. Activation of NADPH Oxidase
- Located in the phagocyte membrane
- Converts O₂ → O₂•⁻ (superoxide radical)
- Uses NADPH as a substrate
- This is the rate-limiting step
NADPH comes from the HMP shunt (via G6PD).
2. Superoxide Dismutation
Enzyme: Superoxide Dismutase (SOD)
- Converts
O₂•⁻ → H₂O₂ (hydrogen peroxide)
3. Formation of Hypochlorite (Bleach)
Enzyme: Myeloperoxidase (MPO) (heme-containing enzyme in neutrophils)
- Uses chloride (Cl⁻)
- Converts
H₂O₂ → HOCl (bleach) - HOCl is a powerful microbicidal agent.
MPO gives a blue-green color to pus and sputum.
4. ROS Neutralization / Antioxidant System
To protect host cells, ROS are neutralized by:
- Catalase
- Glutathione peroxidase
- Glutathione reductase (recycles GSSG → GSH using NADPH)
NADPH is essential for both forming AND removing ROS.
Clinical Correlation
Other Notes
- Pseudomonas aeruginosa produces pyocyanin, a pigment that generates ROS to kill competitors.
- The oxidative burst triggers the release of lysosomal enzymes, thereby amplifying bacterial killing.
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