Tumor necrosis factor primes neutrophils to kill Staphylococcus aureus by an oxygen-dependent mechanism and Plasmodium falciparum by an oxygen-independent mechanism.
AUTOR(ES)
Kowanko, I C
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=174244Documentos Relacionados
- Oxygen-independent intracellular and oxygen-dependent extracellular killing of Escherichia coli S15 by human polymorphonuclear leukocytes.
- Inhibition of Chlamydia psittaci in oxidatively active thioglycolate-elicited macrophages: distinction between lymphokine-mediated oxygen-dependent and oxygen-independent macrophage activation.
- Involvement of superoxide and myeloperoxidase in oxygen-dependent killing of Staphylococcus aureus by neutrophils.
- Susceptibility of Plasmodium falciparum to a peroxidase-mediated oxygen-dependent microbicidal system.
- MprF-Mediated Lysinylation of Phospholipids in Staphylococcus aureus Leads to Protection against Oxygen-Independent Neutrophil Killing
