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[Immunology](https://durgical.com/en/immunology/) · [Innate immunity](https://durgical.com/en/immunology/#a-innate)

# 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

## Key points

- Respiratory burst: NADPH oxidase makes superoxide, then hydrogen peroxide, then hypochlorous acid (myeloperoxidase).
- Chronic granulomatous disease: no NADPH oxidase; catalase-positive organisms and granulomas.
- Diagnosis of chronic granulomatous disease: abnormal DHR flow cytometry (or NBT test).
- Main opsonins: IgG and C3b.
- Chédiak-Higashi: giant granules, albinism, failed phagolysosome fusion.

## 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.

## Memory aid

In chronic granulomatous disease the phagocyte has no matches of its own: it can only burn germs that bring their own hydrogen peroxide. Catalase-positive germs destroy that peroxide and survive.

## 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.

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## Related

- [Innate immunity (overview, barriers)](https://durgical.com/en/immunology/innate-immunity/)
- [Complement: three pathways, MAC, regulators](https://durgical.com/en/immunology/complement-three-pathways-mac-regulators/)
- [Granulomatous inflammation](https://durgical.com/en/immunology/granulomatous-inflammation/)
- [Antigen processing and presentation](https://durgical.com/en/immunology/antigen-processing-and-presentation/)
- [Neutrophil](https://durgical.com/en/immunology/neutrophil/)
- [Monocyte and macrophage](https://durgical.com/en/immunology/monocyte-and-macrophage/)
- [Phagocyte defects: CGD, LAD, Chédiak–Higashi](https://durgical.com/en/immunology/phagocyte-defects-cgd-lad-chediak-higashi/)
- [Spleen: white pulp, red pulp, asplenia](https://durgical.com/en/immunology/spleen-white-pulp-red-pulp-asplenia/)

## Related conditions

- [Chronic granulomatous disease](https://durgical.com/en/conditions/chronic-granulomatous-disease/)

## Microorganisms

- [Staphylococcus aureus](https://durgical.com/en/microbiology/staphylococcus-aureus/)
- [Aspergillus fumigatus](https://durgical.com/en/microbiology/aspergillus-fumigatus/)
- [Nocardia](https://durgical.com/en/microbiology/nocardia/)
- [Mycobacterium tuberculosis](https://durgical.com/en/microbiology/mycobacterium-tuberculosis/)

[← All of immunology](https://durgical.com/en/immunology/)

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](https://openstax.org/books/microbiology/pages/17-4-pathogen-recognition-and-phagocytosis) (OpenStax (Microbiology), 2016); [Chronic granulomatous disease](https://medlineplus.gov/genetics/condition/chronic-granulomatous-disease/) (MedlinePlus Genetics, U.S. National Library of Medicine, 2024).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/immunology/phagocytosis-and-the-respiratory-burst/