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Prepublished online as a Blood First Edition Paper on June 5, 2003; DOI 10.1182/blood-2003-02-0649.
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Blood, 1 October 2003, Vol. 102, No. 7, pp. 2653-2659
PHAGOCYTES
Sex-specific alterations in neutrophil apoptosis: the role of estradiol and progesterone
Eleanor J. Molloy,
Amanda J. O'Neill,
Julie J. Grantham,
Margaret Sheridan-Pereira,
John M. Fitzpatrick,
David W. Webb, and
R. William G. Watson
From the Department of Surgery, Mater Misericordiae University Hospital; Conway Institute of Biomolecular and Biomedical Research, University College Dublin; Department of Paediatrics, Coombe Women's Hospital; and Department of Neurology, Our Lady's Hospital for Sick Children, University College Dublin, Ireland.
Women are conferred with greater immunologic and survival benefits compared to men. Female sex steroids contribute to this sexual dimorphism. Furthermore, during human pregnancy when female sex hormones are elevated, neutrophil apoptosis is delayed. This study examines the specific effects of estradiol and progesterone on neutrophil apoptosis and function in healthy adult men and women. We also examined the contribution of these hormones to the persistence and resolution of an inflammatory response. Spontaneous apoptosis was significantly decreased in women compared with men. Physiologic doses of estradiol and progesterone caused a further delay in spontaneous apoptosis in both men and women but did not diminish Fas antibody-induced apoptosis. The delay in apoptosis was mediated at the level of the mitochondria with decreased release of cytochrome c, which may alter caspase cleavage and activity. There were no associated alterations in neutrophil CD11b, but production of reactive oxygen intermediates (ROIs) in women was increased. Thus, female sex hormones mediate delayed neutrophil apoptosis in both sexes and enhance female intracellular production of ROIs. Modulating hormonal responses may be an effective therapeutic tool in combating inflammatory diseases. (Blood. 2003;102:2653-2659)
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