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Cited by 714Neutrophil, Myeloperoxidase and Oxidative MechanismsCell death mechanisms and regulationPhagocytosis and Immune Regulation

Inhibition of apoptosis and prolongation of neutrophil functional longevity by inflammatory mediators

Lee, Alison, Whyte, Moira K B, Haslett, Christopher·1993·Journal of Leukocyte Biology
DOI 10.1002/jlb.54.4.283
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Abstract

Neutrophil apoptosis leads to macrophage ingestion of intact senescent neutrophils. This may represent a neutrophil removal mechanism that is important both in the control of inflammatory tissue injury and for the normal resolution processes of inflammation. Because apoptosis is likely to be a key control process in cell and tissue homeostasis, a number of inflammatory mediators were tested for their ability to modulate the rate of apoptosis in populations of neutrophils aging in culture. Endotoxic lipopolysaccharide, human recombinant complement factor 5a, and human recombinant granulocyte- macrophage colony-stimulating factor all markedly inhibited the rate of neutrophil apoptosis in a concentration-dependent fashion, without inducing necrosis (as assessed by trypan blue exclusion). This inhibitory effect on the rate of neutrophil apoptosis was shown by morphological criteria and confirmed by gel electrophoresis of extracted DNA. Inhibition of apoptosis of aging neutrophil populations was associated with prolongation of the functional life span of the population as assessed by the ability of neutrophils to spread on glass surfaces, to polarize in response to deliberate stimulation with N-formyl-Met-Leu-Phe (fMLP), and to release the granule enzyme marker myeloperoxidase on fMLP stimulation. These observations show that inflammatory mediators prolong the functional life span of neutrophils through modulation of apoptosis. Further elucidation of these mechanisms will lead to a better understanding of the processes controlling neutrophil residence and function in inflamed tissues and may provide further insights into the molecular mechanisms of apoptosis, which is of widespread importance in tissue biology.

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Crossref · 10.1002/jlb.54.4.283

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  • The release of TNF-α, IL-1β, G-CSF and GM-CSF at the site of macrophage infection increases the survival of recruited neutrophils from 6-12 h to 24-48 h.

    “The release of TNF-α, IL-1β, G-CSF and GM-CSF at the site of macrophage infection increases the survival of recruited neutrophils from 6–12 h to 24–48 h [220].”

    From Superoxide Anion Chemistry—Its Role at the Core of the Innate Immunity (2023) · cites this paper as [220]

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Authors
Lee, A., Whyte, M. K. B., & Haslett, C.
Affiliations
  • University of Edinburgh (GB)
  • Hammersmith Hospital (GB)
Corresponding author
Haslett, Christopher
ORCID
Venue
Journal of Leukocyte Biology
Publisher
Oxford University Press (OUP)
Published
1993-10-01
Volume
54
Issue
4
Pages
283-288
ISSN
  • 0741-5400 (ISSN-L)
  • 1938-3673
DOI
10.1002/jlb.54.4.283
OpenAlex
W2113990199
Cited by
714
References
27
Citations by year
2026: 2 · 2025: 2 · 2024: 5 · 2023: 9 · 2022: 11 · 2021: 12 · 2020: 5 · 2019: 7 · 2018: 9 · 2017: 15 · 2016: 10 · 2015: 19 · 2014: 24 · 2013: 28 · 2012: 12
FWCI
5.84
Type
journal article
Language
en
Open access
closed
Licence
academic.oup.com/pages/standard-publication-reuse-rights (vor)
Locations
  • Journal of Leukocyte Biology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords
neutrophil apoptosis, inflammatory mediators, lipopolysaccharide, GM-CSF, neutrophil clearance, neutrophil polarization, myeloperoxidase release, neutrophil migration, inflammation resolution
MeSH terms
Cell Survival, Cells, Cultured, Chromatin, DNA Damage, Granulocytes, Humans, Inflammation, Lipopolysaccharides, Peroxidase, N-Formylmethionine Leucyl-Phenylalanine, Neutrophils, Recombinant Proteins, Complement C5a, Granulocyte-Macrophage Colony-Stimulating Factor, Cellular Senescence, Apoptosis

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