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Estradiol attenuates lipopolysaccharide-induced CXC chemokine ligand 8 production by human peripheral blood monocytes.

Abstract
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 17beta-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.
AuthorsPatricia A Pioli, Amy L Jensen, Lehn K Weaver, Eyal Amiel, Zheng Shen, Li Shen, Charles R Wira, Paul M Guyre
JournalJournal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 179 Issue 9 Pg. 6284-90 (Nov 01 2007) ISSN: 0022-1767 [Print] United States
PMID17947704 (Publication Type: Journal Article)
Chemical References
  • Interleukin-8
  • Lipopolysaccharides
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Estradiol
Topics
  • Cells, Cultured
  • Endoplasmic Reticulum (drug effects, metabolism)
  • Estradiol (pharmacology)
  • Gene Expression Regulation
  • Humans
  • Interleukin-8 (genetics, metabolism)
  • Lipopolysaccharides (pharmacology)
  • Monocytes (drug effects, metabolism)
  • Neutrophils (drug effects, metabolism)
  • Toll-Like Receptor 4 (metabolism)
  • Transcription, Genetic (genetics)

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