Tumor necrosis factor primes neutrophils to kill Staphylococcus aureus by an oxygen-dependent mechanism and Plasmodium falciparum by an oxygen-independent mechanism.
The 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.
Kowanko
I C
IC
Department of Immunology, University of Adelaide, Australia.
Ferrante
A
A
Clemente
G
G
Kumaratilake
L M
LM
D000818:Animals; D004912:Erythrocytes / Q000469:parasitology; D016166:Free Radical Scavengers / Q000494:pharmacology; D006105:Granulomatous Disease, Chronic / Q000276:immunology*; D006801:Humans; D018375:Neutrophil Activation / Q000187:drug effects*; D010963:Plasmodium falciparum / Q000276:immunology*; D017382:Reactive Oxygen Species; D013211:Staphylococcus aureus / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha