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Nitric Oxide and Infection: Another View


Schoedon, G; Schneemann, M; Walter, R; Blan, N; Hofer, S; Schaffner, A (1995). Nitric Oxide and Infection: Another View. Clinical Infectious Diseases, 21(Supp.):S152-S157.

Abstract

Nitric oxide (NO) has been nicknamed "murderer” and "mediator” because it has toxic and signaling properties. We review these two aspects of NO synthesis from the perspective of the clinical infectious disease specialist by considering the potential of NO as an endothelium-derived relaxing factor (EDRF) in inflammation and sepsis and its potential as an antimicrobial system. We deviate from observations in recent authoritative reviews and point to important speciesdifferences that make it unlikely that NO serves as an EDRF mediating inflammatory vasodilatation in humans or that NO synthesized by human phagocytes has an antimicrobial function.We propose that in humans, NOsynthesis is moreconfined and compartmentalized than in certain other animal species, and therefore, unwelcome toxicity, vasodilatation, or disturbance of paracrine signaling mechanisms (i.e., modulation of phagocytic cell functions) are avoided during inflammation

Abstract

Nitric oxide (NO) has been nicknamed "murderer” and "mediator” because it has toxic and signaling properties. We review these two aspects of NO synthesis from the perspective of the clinical infectious disease specialist by considering the potential of NO as an endothelium-derived relaxing factor (EDRF) in inflammation and sepsis and its potential as an antimicrobial system. We deviate from observations in recent authoritative reviews and point to important speciesdifferences that make it unlikely that NO serves as an EDRF mediating inflammatory vasodilatation in humans or that NO synthesized by human phagocytes has an antimicrobial function.We propose that in humans, NOsynthesis is moreconfined and compartmentalized than in certain other animal species, and therefore, unwelcome toxicity, vasodilatation, or disturbance of paracrine signaling mechanisms (i.e., modulation of phagocytic cell functions) are avoided during inflammation

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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:610 Medicine & health
Scopus Subject Areas:Health Sciences > Microbiology (medical)
Health Sciences > Infectious Diseases
Language:English
Date:1 October 1995
Deposited On:12 Oct 2018 08:07
Last Modified:31 Jul 2020 02:21
Publisher:Oxford University Press
ISSN:1058-4838
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/clinids/21.supplement_2.s152
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicenceoxford101093clinids21Supplement_2S152 (Library Catalogue)

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