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Please use this identifier to cite or link to this item: https://hdl.handle.net/2440/14640
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dc.contributor.authorKowanko, I.-
dc.contributor.authorFerrante, A.-
dc.contributor.authorClemente, G.-
dc.contributor.authorKumaratilake, L.-
dc.date.issued1996-
dc.identifier.citationInfection and Immunity, 1996; 64(8):3435-3437-
dc.identifier.issn0019-9567-
dc.identifier.issn1098-5522-
dc.identifier.urihttp://hdl.handle.net/2440/14640-
dc.description.abstractThe cytokine tumor necrosis factor (TNF) plays the important role of priming neutrophils for increased antimicrobial activity. We now demonstrate that human neutrophils which lack the ability to generate oxygen radicals, from patients with chronic granulomatous disease, show TNF-induced enhancement of killing of intraerythrocytic stages of Plasmodium falciparum but not of Staphylococcus aureus.-
dc.description.statementofresponsibilityI. C. Kowanko, A. Ferrante, G. Clemente and L. M. Kumaratilake-
dc.language.isoen-
dc.publisherAMER SOC MICROBIOLOGY-
dc.rightsCopyright © 1996, American Society for Microbiology-
dc.source.urihttp://iai.asm.org/cgi/content/abstract/64/8/3435-
dc.subjectErythrocytes-
dc.subjectAnimals-
dc.subjectHumans-
dc.subjectPlasmodium falciparum-
dc.subjectStaphylococcus aureus-
dc.subjectGranulomatous Disease, Chronic-
dc.subjectReactive Oxygen Species-
dc.subjectTumor Necrosis Factor-alpha-
dc.subjectFree Radical Scavengers-
dc.subjectNeutrophil Activation-
dc.titleTumor necrosis factor primes neutrophils to kill Staphylococcus aureus by an oxygen-dependent mechanism and Plasmodium falciparum by an oxygen-independent mechanism-
dc.typeJournal article-
dc.identifier.doi10.1128/iai.64.8.3435-3437.1996-
pubs.publication-statusPublished-
dc.identifier.orcidFerrante, A. [0000-0002-2581-6407]-
Appears in Collections:Aurora harvest 2
Nursing publications

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