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 Blood, 15 January 2008, Vol. 111, No. 2, pp. 878-884.
Prepublished online as a Blood First Edition Paper on October 17, 2007; DOI 10.1182/blood-2007-05-087833.

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PHAGOCYTES

The dual effects of TNF{alpha} on neutrophil apoptosis are mediated via differential effects on expression of Mcl-1 and Bfl-1

Andrew Cross1, Robert J. Moots2, and Steven W. Edwards1

1 School of Biological Sciences, Biosciences Building, and 2 School of Clinical Sciences, University of Liverpool, Liverpool, United Kingdom

Neutrophils have a very short half-life in the circulation, undergoing rapid death by apoptosis, but a number of agents can either delay or accelerate the rate at which these cells undergo death. TNF{alpha} can exert opposing, concentration-dependent effects on neutrophils to either accelerate their apoptosis or enhance their survival. We show that TNF{alpha} greatly increases the rate of turnover of Mcl-1, an antiapoptotic protein that plays a key role in neutrophil survival. In contrast to Mcl-1 turnover in control- or granulocyte-macrophage colony-stimulating factor (GM-CSF)–treated neutrophils that occurs via the proteasome, TNF{alpha}-accelerated Mcl-1 turnover occurs via activation of caspases. Mcl-1–depleted cells thus have accelerated rates of apoptosis. While TNF{alpha} had no effect on MCL-1 transcription, it induced expression of another antiapoptotic molecule, BFL-1. Low concentrations of TNF{alpha} (≤ 1 ng/mL) stimulated BFL-1 expression, whereas higher concentrations (≥ 10 ng/mL) triggered caspase-dependent acceleration of Mcl-1 turnover. These opposing effects on 2 separate antiapoptotic systems of neutrophils explain the divergent effects of TNF{alpha} on neutrophil apoptosis and have important implications for understanding how TNF{alpha} may affect immune function in inflammatory diseases.


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