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Article: Endotoxin induction of tumor necrosis factor is enhanced by acid-labile interferon-α in acquired immunodeficiency syndrome

TitleEndotoxin induction of tumor necrosis factor is enhanced by acid-labile interferon-α in acquired immunodeficiency syndrome
Authors
Issue Date1989
PublisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org
Citation
Journal Of Clinical Investigation, 1989, v. 84 n. 3, p. 738-743 How to Cite?
AbstractHigh levels of an acid-labile IFN-α have been demonstrated in the sera of patients with symptomatic HIV infection. IFNs have been shown to enhance the cytotoxic and antiproliferative actions of tumor necrosis factor (TNF), which is a potent mediator of inflammation and sepsis. We show that the acid-labile IFN-α present in AIDS sera can induce TNF synthesis and sensitize blood monocytes (BM) to endotoxin stimulation resulting in further synthesis of TNF in vitro. TNF production by BM from patients with HIV infections and normal controls was measured by a cytotoxicity assay on L929 cells using human TNFα as a standard. BM from AIDS patients spontaneously produce high levels of TNF and are hypersensitive to endotoxin stimulation, resulting in enhanced synthesis of TNF. In determining the mechanism involved, we demonstrated that treatment of normal BM with AIDS sera results in induction of TNF. Neutralization of the acid-bile IFN-α in AIDS sera with polyclonal anti-IFN-α antibodies results in diminution of TNF induction. In addition, pretreatment of normal BM with AIDS sera, IFN-α, or IFN-γ renders the cells hypersensitive to endotoxin. Consequently, activation of the TNF system by the acid-labile IFN-α contributes to some of the physiological disturbances, such as the wasting syndrome, and to the pathophysiology of sepsis in AIDS patients.
Persistent Identifierhttp://hdl.handle.net/10722/170236
ISSN
2015 Impact Factor: 12.575
2015 SCImago Journal Rankings: 8.764
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLau, ASen_US
dc.contributor.authorLivesey, JFen_US
dc.date.accessioned2012-10-30T06:06:53Z-
dc.date.available2012-10-30T06:06:53Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Clinical Investigation, 1989, v. 84 n. 3, p. 738-743en_US
dc.identifier.issn0021-9738en_US
dc.identifier.urihttp://hdl.handle.net/10722/170236-
dc.description.abstractHigh levels of an acid-labile IFN-α have been demonstrated in the sera of patients with symptomatic HIV infection. IFNs have been shown to enhance the cytotoxic and antiproliferative actions of tumor necrosis factor (TNF), which is a potent mediator of inflammation and sepsis. We show that the acid-labile IFN-α present in AIDS sera can induce TNF synthesis and sensitize blood monocytes (BM) to endotoxin stimulation resulting in further synthesis of TNF in vitro. TNF production by BM from patients with HIV infections and normal controls was measured by a cytotoxicity assay on L929 cells using human TNFα as a standard. BM from AIDS patients spontaneously produce high levels of TNF and are hypersensitive to endotoxin stimulation, resulting in enhanced synthesis of TNF. In determining the mechanism involved, we demonstrated that treatment of normal BM with AIDS sera results in induction of TNF. Neutralization of the acid-bile IFN-α in AIDS sera with polyclonal anti-IFN-α antibodies results in diminution of TNF induction. In addition, pretreatment of normal BM with AIDS sera, IFN-α, or IFN-γ renders the cells hypersensitive to endotoxin. Consequently, activation of the TNF system by the acid-labile IFN-α contributes to some of the physiological disturbances, such as the wasting syndrome, and to the pathophysiology of sepsis in AIDS patients.en_US
dc.languageengen_US
dc.publisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.orgen_US
dc.relation.ispartofJournal of Clinical Investigationen_US
dc.subject.meshAcquired Immunodeficiency Syndrome - Metabolismen_US
dc.subject.meshAdjuvants, Immunologic - Physiologyen_US
dc.subject.meshAdulten_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndotoxins - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshHydrogen-Ion Concentrationen_US
dc.subject.meshInterferon Type I - Physiologyen_US
dc.subject.meshInterferon-Gamma - Pharmacologyen_US
dc.subject.meshLipopolysaccharides - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshMonocytes - Metabolismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Biosynthesisen_US
dc.titleEndotoxin induction of tumor necrosis factor is enhanced by acid-labile interferon-α in acquired immunodeficiency syndromeen_US
dc.typeArticleen_US
dc.identifier.emailLau, AS:asylau@hku.hken_US
dc.identifier.authorityLau, AS=rp00474en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1172/JCI114231-
dc.identifier.pmid2503543-
dc.identifier.scopuseid_2-s2.0-0024429144en_US
dc.identifier.volume84en_US
dc.identifier.issue3en_US
dc.identifier.spage738en_US
dc.identifier.epage743en_US
dc.identifier.isiWOS:A1989AN25900004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLau, AS=7202626202en_US
dc.identifier.scopusauthoridLivesey, JF=36786064400en_US

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