Phagocytosis and the respiratory burst !
- Process
How neutrophils and macrophages swallow microbes and kill them with acid, enzymes and bleach-like oxygen products.
Updated 2026-11-01
What it is
Phagocytosis is the uptake of microbes or debris into a membrane vesicle (phagosome) that fuses with lysosomes. Killing relies on oxygen-dependent mechanisms (the respiratory burst, driven by NADPH oxidase) and oxygen-independent ones (lysozyme, defensins, proteases, acid). Defects in this machinery cause specific patterns of infection, most famously chronic granulomatous disease.
Key facts
- IgG and C3b are the main opsonins.
- Macrophages also make nitric oxide through inducible NO synthase, especially when activated by IFN-γ.
- Neutrophils can release extracellular traps (NETs) of DNA and granule proteins.
- Some microbes resist killing, for example Mycobacterium tuberculosis, which blocks phagosome maturation.
Step by step
- Recognition: pattern receptors or opsonin receptors (Fc receptors for IgG, complement receptors for C3b) bind the microbe.
- Engulfment: pseudopods surround the microbe and close into a phagosome.
- The phagosome fuses with lysosomes to form a phagolysosome and becomes acidic.
- Respiratory burst: NADPH oxidase transfers electrons to oxygen and makes superoxide.
- Superoxide dismutase converts superoxide into hydrogen peroxide.
- Myeloperoxidase (neutrophils) uses hydrogen peroxide and chloride to make hypochlorous acid, a potent oxidant.
- Lysosomal enzymes digest the microbe; macrophages and dendritic cells can present peptides from it to T cells.
Clinical notes
- Chronic granulomatous disease: NADPH oxidase defect (most often X-linked, CYBB gene); recurrent infections with catalase-positive organisms such as Staphylococcus aureus, Aspergillus, Nocardia, Serratia and Burkholderia, plus granulomas.
- Myeloperoxidase deficiency: usually mild; increased risk of Candida infections.
- Chédiak-Higashi syndrome (LYST gene): giant granules, defective phagolysosome fusion, partial albinism and recurrent pyogenic infections.
- Asplenia removes a major site of phagocytosis of opsonized encapsulated bacteria.
In the lab
- Dihydrorhodamine (DHR) flow cytometry test: no fluorescence after stimulation in chronic granulomatous disease.
- Nitroblue tetrazolium test: the older test; it stays colorless when NADPH oxidase does not work.
Test yourself
Think of the answer, then tap the question to see it.
Which enzyme starts the respiratory burst, and what does it produce?
NADPH oxidase, which transfers electrons to molecular oxygen to make superoxide.
Why do patients with chronic granulomatous disease suffer mainly from catalase-positive organisms?
Their phagocytes cannot make their own oxidants; catalase-positive microbes break down the hydrogen peroxide they produce, so the phagocyte has nothing to use against them.
Which laboratory test is used to screen for chronic granulomatous disease?
The dihydrorhodamine flow cytometry test (or the older nitroblue tetrazolium test), which shows absent oxidative burst.
What is the role of myeloperoxidase?
In neutrophil granules it combines hydrogen peroxide with chloride to form hypochlorous acid, a strong microbicide.
Related
- Innate immunity (overview, barriers)
- Complement: three pathways, MAC, regulators
- Granulomatous inflammation
- Antigen processing and presentation
- Neutrophil
- Monocyte and macrophage
- Phagocyte defects: CGD, LAD, Chédiak–Higashi
- Spleen: white pulp, red pulp, asplenia
Related conditions
Microorganisms
Educational content on the immune system; not a treatment or individual vaccination guide and no substitute for a health professional's advice. No doses are given.
Sources: 17.4 Pathogen Recognition and Phagocytosis (OpenStax (Microbiology), 2016); Chronic granulomatous disease (MedlinePlus Genetics, U.S. National Library of Medicine, 2024).
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Representative model, for educational purposes only.