Header

UZH-Logo

Maintenance Infos

Nitric oxide synthase is not a constituent of the antimicrobial armature of human mononuclear phagocytes


Schneemann, M; Schoedon, G; Hofer, S; Blau, N; Guerrero, L; Schaffner, A (1993). Nitric oxide synthase is not a constituent of the antimicrobial armature of human mononuclear phagocytes. Journal of Infectious Diseases, 167(6):1358-1363.

Abstract

Nitric oxide synthase (NOS) has received immense interest as an antimicrobial and antitumoral effector system of mononuclear phagocytes from rodents. Because there is increasing doubt that an analogous system exists in human macrophages, NOS was reexamined in these cells. Under tightly controlled conditions, with murine macrophages as positive controls, human macrophages failed to secrete nitric oxide <0.1µmol/106 cells/24 h), even after activation with endotoxin, intcrferon-γ, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor- a, bacteria, or proliferating lymphocytes. The discrepancy between murine and human macrophages depended on neither the anatomic source (blood, peritoneum), the agent used for activation, nor the duration of activation. NOS activity was paralleled by metabolization of L-arginine to L-citrulline. Exogenous tetrahydrobiopterin, an essential cofactor of NOS not synthesized by human macrophages, did not support NOS activity in human macrophages. Also, no NOS activity was found in cellular subfractions of human macrophages. It appears that in humans, the inducible high-output NOS is not conserved as an antimicrobial system of macrophages

Abstract

Nitric oxide synthase (NOS) has received immense interest as an antimicrobial and antitumoral effector system of mononuclear phagocytes from rodents. Because there is increasing doubt that an analogous system exists in human macrophages, NOS was reexamined in these cells. Under tightly controlled conditions, with murine macrophages as positive controls, human macrophages failed to secrete nitric oxide <0.1µmol/106 cells/24 h), even after activation with endotoxin, intcrferon-γ, granulocyte-macrophage colony-stimulating factor, tumor necrosis factor- a, bacteria, or proliferating lymphocytes. The discrepancy between murine and human macrophages depended on neither the anatomic source (blood, peritoneum), the agent used for activation, nor the duration of activation. NOS activity was paralleled by metabolization of L-arginine to L-citrulline. Exogenous tetrahydrobiopterin, an essential cofactor of NOS not synthesized by human macrophages, did not support NOS activity in human macrophages. Also, no NOS activity was found in cellular subfractions of human macrophages. It appears that in humans, the inducible high-output NOS is not conserved as an antimicrobial system of macrophages

Statistics

Citations

Dimensions.ai Metrics
302 citations in Web of Science®
292 citations in Scopus®
Google Scholar™

Altmetrics

Downloads

12 downloads since deposited on 09 Oct 2018
12 downloads since 12 months
Detailed statistics

Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:1 June 1993
Deposited On:09 Oct 2018 14:16
Last Modified:24 Nov 2018 02:53
Publisher:Oxford University Press
ISSN:0022-1899
OA Status:Green
Free access at:Publisher DOI. An embargo period may apply.
Publisher DOI:https://doi.org/10.1093/infdis/167.6.1358
Related URLs:https://www.swissbib.ch/Search/Results?lookfor=nationallicenceoxford101093infdis16761358 (Library Catalogue)
PubMed ID:7684756

Download

Download PDF  'Nitric oxide synthase is not a constituent of the antimicrobial armature of human mononuclear phagocytes'.
Preview
Content: Published Version
Language: English
Filetype: PDF (Nationallizenz 142-005)
Size: 681kB
View at publisher