Cited by 503Neutrophil, Myeloperoxidase and Oxidative MechanismsMetabolism, Diabetes, and CancerCancer, Hypoxia, and Metabolism

Energy Metabolism of Human Neutrophils during Phagocytosis

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Borregaard, Niels, Herlin, Troels·1982·Journal of Clinical Investigation

Abstract

Detailed quantitative studies were performed on the generation and utilization of energy by resting and phagocytosing human neutrophils. The ATP content was 1.9 fmol/cell, was constant during rest, and was not influenced by the presence or absence of glucose in the medium. The intracellular content of phosphocreatine was less than 0.2 fmol/cell. In the presence of glucose, ATP was generated almost exclusively from lactate produced from glucose taken up from the surrounding medium. The amount of lactate produced could account for 85% of the glucose taken up by the cells, and the intracellular glycosyl store, glycogen, was not drawn upon. The rate of ATP generation as calculated from the rate of lactate production was 1.3 fmol/cell/min. During phagocytosis, there was no measurable increase in glucose consumption or lactate production, and the ATP content fell rapidly to 0.8 fmol/cell. This disappearance of ATP was apparently irreversible since no corresponding increase in ADP or AMP was observed. It therefore appears that this phagocytosis-induced fall in ATP concentration represents all the extra energy utilized in human neutrophils in the presence of glucose. In the absence of glucose, the rate of ATP generation in the resting cell was considerably smaller, 0.75 fmol/cell per min, as calculated from the rate of glycolysis, which is sustained exclusively by glycogenolysis. Under this condition, however, phagocytosis induces significant enhancement of glycogenolysis and the rate of lactate production is increased by 60%, raising the rate of ATP generation to 1.2 fmol/cell per min. Nonetheless, the ATP content drops significantly from 1.9 to 1.0 fmol/cell. Neutrophils from patients with chronic granulomatous disease have the same rate of glycolysis and the same ATP content as normal cells, thus confirming that the defective respiration of these cells does not affect their energy metabolism.

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  • PMNs are primarily glycolytic cells, with few mitochondria and little energy produced from respiration.

    “It has long been known that PMNs are primarily glycolytic cells, with few mitochondria and little energy produced from respiration6.”

    From Hypoxia: an alarm signal during intestinal inflammation (2010) · cites this paper as [6]

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  1. Bergmeyer, H. U. 1974. In Methods of Enzymatic Anal- ysis. Verlag Chemie Weinheim. Academic Press, Inc., New York. p. 1464-1467.

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Authors
Borregaard, N., & Herlin, T.
Affiliations
Marselisborgcentret (DK)
Venue
Journal of Clinical Investigation
Published
1982-09-01
Volume
70
Issue
3
Pages
550-557
ISSN
0021-9738 (ISSN-L)
OpenAlex
W2151593963
Cited by
503
References
36
Citations by year
2026: 17 · 2025: 28 · 2024: 23 · 2023: 32 · 2022: 35 · 2021: 34 · 2020: 36 · 2019: 34 · 2018: 22 · 2017: 26 · 2016: 19 · 2015: 12 · 2014: 19 · 2013: 17 · 2012: 15
FWCI
2.92
Type
journal article
Language
en
Open access
Locations
  • Journal of Clinical Investigation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Sundhed og Sygdom, Det Frie Forskningsråd
  • Medical Research Council
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Keywords
neutrophils, phagocytosis, energy metabolism, ATP production, lactic acid production, glycolysis, glycogenolysis, glucose uptake, phosphocreatine, chronic granulomatous disease, respiratory defects
MeSH terms
Adenine Nucleotides, Adenosine Triphosphate, Energy Metabolism, Glucose, Glycogen, Glycolysis, Granulomatous Disease, Chronic, Humans, Neutrophils, Phagocytosis, Phosphocreatine

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