Tissue Destruction by Neutrophils
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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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].”
From Oral neutrophils are an independent marker of the systemic inflammatory response after cardiac bypass (2014) · cites this paper as [23]
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BackgroundInfluentialModifications of IL-6 by Hypochlorous Acids: Effects on Receptor Binding
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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
- Publisher
- Massachusetts Medical Society
- 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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