Cited by 3,950Neutrophil, Myeloperoxidase and Oxidative MechanismsProtease and Inhibitor MechanismsInflammation biomarkers and pathways

Tissue Destruction by Neutrophils

Epstein, Franklin H., Weiss, Stephen J.·1989·New England Journal of Medicine

Abstract

WITH increasing frequency, the human neutrophil is being implicated as a mediator of tissue-destructive events in inflammatory diseases ranging from rheumatoid arthritis and myocardial reperfusion injury to respiratory distress syndromes, blistering skin disorders, and ulcerative colitis.1 , 2 In each of these diseases, as well as a variety of other acute inflammatory disorders, important components of these pathologic processes are being linked to the neutrophil's ability to release a complex assortment of agents that can destroy normal cells and dissolve connective tissues. Although these toxins normally defend the host against invading microbes, the neutrophil has little intrinsic ability to differentiate between foreign . . .

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Crossref · 10.1056/nejm198902093200606

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78 of 78 references verified0 citation errors · 0 not checkable

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  • An excessive PMN response has previously been implicated in the pathogenesis of capillary leak syndromes resulting in decreased perfusion and end-organ damage, including acute respiratory distress syndrome and MOF.

    “whereas an excessive PMN response has previously been implicated in the pathogenesis of capillary leak syndromes resulting in decreased perfusion and end-organ damage, including acute respiratory distress syndrome and MOF [22-24].”

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Authors
Epstein, F. H., & Weiss, S. J.
Affiliations
University of Michigan (US)
Corresponding author
Epstein, Franklin H.
Venue
New England Journal of Medicine
Published
1989-02-09
Volume
320
Issue
6
Pages
365-376
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W2072796605
Cited by
3,950
References
78
Citations by year
2026: 13 · 2025: 31 · 2024: 39 · 2023: 42 · 2022: 35 · 2021: 54 · 2020: 51 · 2019: 49 · 2018: 56 · 2017: 53 · 2016: 68 · 2015: 65 · 2014: 81 · 2013: 81 · 2012: 92
FWCI
22.38
Type
journal article
Language
en
Open access
closed
Locations
  • New England Journal of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Heart, Lung, and Blood Institute (HL-28024)
  • National Institute of Allergy and Infectious Diseases (AI23876, AI 21301)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Protease and Inhibitor Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
neutrophils, tissue destruction, neutrophilic inflammation, rheumatoid arthritis, myocardial ischemia-reperfusion injury, respiratory distress syndrome, blistering skin disease, ulcerative colitis, acute inflammation
MeSH terms
Animals, Humans, Hypochlorous Acid, Inflammation, NADH, NADPH Oxidoreductases, Neutrophils, Oxygen, NADPH Oxidases

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