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Estradiol Attenuates Lipopolysaccharide-Induced CXC Chemokine Ligand 8 Production by Human Peripheral Blood Monocytes

Patricia A. Pioli^1,*, Amy L. Jensen^*, Lehn K. Weaver, Eyal Amiel, Zheng Shen, Li Shen, Charles R. Wira^* and Paul M. Guyre^*,

^* Department of Physiology and Department of Immunology and Microbiology, Dartmouth Medical School, Lebanon, NH 03756

Regulation of the inflammatory response is imperative to the maintenance of immune homeostasis. Activated monocytes elaborate a broad variety of proinflammatory cytokines that mediate inflammation, including CXCL8. Release of this chemokine attracts neutrophils to sites of bacterial invasion and inflammation; however, high levels of CXCL8 may result in excessive neutrophil infiltration and subsequent tissue damage. In this study, we demonstrate that 17-estradiol (E2) attenuates LPS-induced expression of CXCL8 in human peripheral blood monocytes. Treatment of monocytes with estradiol before administration of LPS reduces CXCL8 message and protein production through an estrogen receptor-dependent mechanism, and luciferase reporter assays demonstrate that this inhibition is mediated transcriptionally. Importantly, the ability of estradiol-pretreated LPS-activated monocytes to mobilize neutrophils is impaired. These results implicate a role for estradiol in the modulation of the immune response, and may lead to an enhanced understanding of gender-based differences in inflammatory control mechanisms.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Address correspondence and reprint requests to Dr. Patricia A. Pioli, Department of Physiology, Dartmouth Medical School, Lebanon, NH 03756. E-mail address: pioli{at}dartmouth.edu

² Abbreviations used in this paper: ER, estrogen receptor; CM, conditioned medium; ARE, AU-rich element.

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