Document Detail


Neuroendocrine circuitry and endometriosis: progesterone derivative dampens corticotropin-releasing hormone-induced inflammation by peritoneal cells in vitro.
MedLine Citation:
PMID:  19898767     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Clinical symptoms of endometriosis, such as pain and infertility, can be described as persistent stressors. Such continuous exposure to stress may severely affect the equilibrium and bidirectional communication of the endocrine and immune system, hereby further aggravating the progression of endometriosis. In the present study, we aimed to tease apart mediators that are involved in the stress response as well as in the progression of endometriosis. Women undergoing diagnostic laparoscopy due to infertility were recruited (n = 69). Within this cohort, early stage of endometriosis were diagnosed in n = 30 and advanced stage of endometriosis in n = 8. Levels of progesterone in serum were determined. Frequency of progesterone receptor (PR) expression on CD56(+) and CD8(+) peritoneal lymphocytes was analysed by flow cytometry. The production of tumour necrosis factor (TNF) and interleukin (IL)-10 by peritoneal leukocytes upon stimulation with the potent stress mediator corticotropin-releasing hormone (CRH) and the progesterone derivative dydrogesterone, or both, were evaluated. Furthermore, the production of progesterone-induced blocking factor (PIBF) by peritoneal leukocytes and the expression of PR in endometriotic tissue were investigated. Levels of progesterone in serum were decreased in women with endometriosis and inversely correlated to pain scores. Furthermore, an increased frequency of CD56(+)PR(+) and CD8(+)PR(+) peritoneal lymphocytes was present in advanced endometriosis. The TNF/IL-10 ratio, reflecting cytokine secretion by peritoneal cells, was higher in cells derived from endometriosis patients and could be further heightened by CRH stimulation, whereas stimulation with dydrogesterone abrogated the CRH-mediated inflammation. Finally, the expression of PIBF by peritoneal leukocytes was increased in endometriosis. Low levels of progesterone in the follicular phase could be responsible for the progression of endometriosis and related pain. Peripheral CRH, increasing upon high psychological stress, might contribute to the peritoneal inflammation present in endometriosis. The therapeutic application of progesterone derivatives, CRH blocking agents as well as improvement of stress coping may disrupt the vicious circle between the chronic peritoneal inflammation and high perception of psychological stress in endometriosis.
Authors:
Nadja Tariverdian; Mirjam Rücke; Julia Szekeres-Bartho; Sandra M Blois; Eva F Karpf; Peter Sedlmayr; Burghard F Klapp; Heribert Kentenich; Friederike Siedentopf; Petra C Arck
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-11-08
Journal Detail:
Title:  Journal of molecular medicine (Berlin, Germany)     Volume:  88     ISSN:  1432-1440     ISO Abbreviation:  J. Mol. Med.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-11     Completed Date:  2010-06-22     Revised Date:  2011-07-08    
Medline Journal Info:
Nlm Unique ID:  9504370     Medline TA:  J Mol Med (Berl)     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  267-78     Citation Subset:  IM    
Affiliation:
Center of Internal Medicine and Dermatology, Division of PsychoNeuroImmunology, Charité, Universitätsmedizin Berlin, Campus Virchow, Augustenburger Platz 1, Berlin, Germany.
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MeSH Terms
Descriptor/Qualifier:
Adult
Cells, Cultured
Cohort Studies
Corticotropin-Releasing Hormone / antagonists & inhibitors,  pharmacology*
Dydrogesterone / pharmacology*
Endometriosis / immunology*,  metabolism,  pathology
Female
Humans
Inflammation Mediators / metabolism*
Interleukin-10 / metabolism
Neurosecretory Systems / metabolism
Peritoneum / cytology
Phenotype
Progesterone / blood
Tumor Necrosis Factor-alpha / metabolism
Chemical
Reg. No./Substance:
0/Inflammation Mediators; 0/Tumor Necrosis Factor-alpha; 130068-27-8/Interleukin-10; 152-62-5/Dydrogesterone; 57-83-0/Progesterone; 9015-71-8/Corticotropin-Releasing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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