Nitric oxide attenuates beryllium-induced IFNgamma responses in chronic beryllium disease : evidence for mechanisms independent of IL-18

(c) 2002 Elsevier Science (USA).

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 103(2002), 2 vom: 07. Mai, Seite 169-75
1. Verfasser: Barna, Barbara P (VerfasserIn)
Weitere Verfasser: Dweik, Raed A, Farver, Carol F, Culver, Daniel, Yen-Lieberman, Belinda, Thomassen, Mary Jane
Format: Aufsatz
Sprache:English
Veröffentlicht: 2002
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Caspase Inhibitors Cysteine Proteinase Inhibitors Interleukin-18 Nitric Oxide Donors Nitroso Compounds Oligopeptides L 709049 143313-51-3 2,2'-(hydroxynitrosohydrazono)bis-ethanamine mehr... 146724-94-9 Nitric Oxide 31C4KY9ESH Interferon-gamma 82115-62-6 Beryllium OW5102UV6N
Beschreibung
Zusammenfassung:(c) 2002 Elsevier Science (USA).
In chronic beryllium disease (CBD), a granulomatous lung disease characterized by hypersensitivity to beryllium salts (BE), BE challenge of bronchoalveolar lavage cells induces IFNgamma. Although nitric oxide (NO) is elevated in CBD airways, the effects of NO on CBD IFNgamma responses are unknown. Here we report that BE-stimulated IFNgamma production in CBD lavage cells was markedly reduced (74%) by the NO generator DETA NONOate. Investigation of IFNgamma-stimulatory cytokine involvement indicated that lavage cell IL-18 was significantly increased (fourfold) by BE and reduced (64%) by DETA NONOate but IL-12 was undetectable. IL-18 production was caspase-1-dependent but caspase 1 inhibition reduced IFNgamma only partially (43%). Specific antibody depletion of lavage cell IL-18 yielded marginal reduction (19%) of IFNgamma. Data are the first to show that: (1) BE stimulates IL-18 as well as IFNgamma in CBD; (2) BE cytokine responses are NO-sensitive; and (3) NO down-regulation of IFNgamma involves other sites in addition to IL-18
Beschreibung:Date Completed 01.07.2002
Date Revised 20.11.2014
published: Print
Citation Status MEDLINE
ISSN:1521-7035