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

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 inf...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2007-11, Vol.179 (9), p.6284-6290
Main Authors: Pioli, Patricia A, Jensen, Amy L, Weaver, Lehn K, Amiel, Eyal, Shen, Zheng, Shen, Li, Wira, Charles R, Guyre, Paul M
Format: Article
Language:English
Subjects:
Cells, Cultured
Endoplasmic Reticulum - drug effects
Endoplasmic Reticulum - metabolism
Estradiol - pharmacology
Gene Expression Regulation
Humans
Interleukin-8 - genetics
Interleukin-8 - metabolism
Lipopolysaccharides - pharmacology
Monocytes - drug effects
Monocytes - metabolism
Neutrophils - drug effects
Neutrophils - metabolism
Toll-Like Receptor 4 - metabolism
Transcription, Genetic - genetics
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Summary: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.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.179.9.6284