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Analysis of the mechanisms involved in the stimulation of neutrophil apoptosis by tumour necrosis factor‐α
Author(s) -
Salamone Gabriela,
Trevani Analía,
Martínez Diego,
Vermeulen Mónica,
Gamberale Romina,
FernándezCalotti Paula,
Raiden Silvina,
Giordano Mirta,
Geffner Jorge
Publication year - 2004
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2004.01973.x
Subject(s) - apoptosis , tumor necrosis factor alpha , zymosan , stimulation , immunology , caspase , microbiology and biotechnology , necrosis , biology , cytokine , inflammation , programmed cell death , granulocyte , cancer research , endocrinology , biochemistry , in vitro , genetics
Summary We have previously reported that human neutrophils pretreated with tumour necrosis factor‐α (TNF‐α) and then exposed to a variety of agents such as immune complexes, zymosan, phorbol 12‐myristate 13‐acetate (PMA), C5a, fMLP, or granulocyte–macrophage colony‐stimulating factor (GM‐CSF), undergo a dramatic stimulation of apoptosis, suggesting that TNF‐α is able to prime an apoptotic death programme which can be rapidly triggered by different stimuli. We report here that this response involves the participation of Mac‐1 (CD11b/CD18), is dependent on caspases 3, 8 and 9, and is associated with both a loss of mitochondrial transmembrane potential and a down‐regulation in expression of the anti‐apoptotic protein, Mcl‐1. Interestingly, we also found that the anti‐apoptotic cytokine interleukin‐1 (IL‐1) improves the ability of TNF‐α to promote apoptosis, supporting the notion than TNF‐α, acting together with IL‐1, may favour the depletion of neutrophils from the inflammatory areas during the course of acute inflammation.