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Article ; Online: Environmental immune disruption: a comorbidity factor for reproduction?

Rier, Sherry E

2008 Volume 89, Issue 2 Suppl, Page(s) e103–8

Abstract: Objective: To review the evidence on exposure to environmental contaminants and immune system disruption, and how this has been demonstrated or hypothesized to impact reproductive health and fertility.: Design: Review of literature.: Result(s): ... ...

Abstract	Objective: To review the evidence on exposure to environmental contaminants and immune system disruption, and how this has been demonstrated or hypothesized to impact reproductive health and fertility. Design: Review of literature. Result(s): Exposure to environmental contaminants including polyhalogenated aromatic hydrocarbons, heavy metals, and other hormone disrupting chemicals are associated with a wide spectrum of effects on the reproductive, immune, and endocrine systems. Of particular importance is the potential impact of environmental chemicals on the mucosal immune system of the human female reproductive tract. Immune cells within the reproductive tract produce cytokines and chemokines in response to estrogen and progesterone, thereby influencing various reproductive processes including ovulation, sperm migration, fertilization, implantation, endometrial remodeling, and immune response to infectious challenge. Recent research in animals and humans indicates a potential association between exposure to dioxins, endometriosis, and disruption of the immune system. Studies have shown that rhesus monkeys exposed to dioxins with elevated serum levels of certain toxic coplanar PCBs and an increased total serum toxic equivalency had a high prevalence of endometriosis, and the severity of disease correlated with serum concentrations of PCB77. Dioxin-exposed animals with endometriosis showed long-term alterations in immunity associated with elevated levels of dioxin and specific coplanar dioxin-like congeners. Conclusion(s): Perspectives on the potential mechanism(s) of toxicity induced by environmental chemicals in endometriosis and other reproductive diseases, important knowledge needs, potential animal models, and considerations integral to future studies are discussed.
MeSH term(s)	Animals ; Comorbidity ; Endometriosis/chemically induced ; Endometriosis/epidemiology ; Endometriosis/immunology ; Environmental Pollutants/toxicity ; Female ; Humans ; Immune System Diseases/chemically induced ; Immune System Diseases/epidemiology ; Reproduction/immunology
Chemical Substances	Environmental Pollutants
Language	English
Publishing date	2008-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80133-1
ISSN	1556-5653 ; 0015-0282
ISSN (online)	1556-5653
ISSN	0015-0282
DOI	10.1016/j.fertnstert.2007.12.040
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Article: The potential role of exposure to environmental toxicants in the pathophysiology of endometriosis.

Rier, Sherry E

Annals of the New York Academy of Sciences

2002 Volume 955, Page(s) 201–12; discussion 230–2, 396–406

Abstract: Humans and animals are exposed daily to a complex mixture of polyhalogenated aromatic hydrocarbons (PHAHs). Previous work has shown that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with a dose-dependent increase in the incidence ... ...

Abstract	Humans and animals are exposed daily to a complex mixture of polyhalogenated aromatic hydrocarbons (PHAHs). Previous work has shown that exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with a dose-dependent increase in the incidence and severity of endometriosis in the rhesus monkey. Dioxin-like chemicals can also exert effects in combination with TCDD via the aryl hydrocarbon receptor. Using a rhesus model of chronic TCDD exposure and endometriosis, serum concentrations of TCDD and 19 dioxin-like PHAHs were quantified 13 years after termination of exposure to TCDD. In additional studies, the immune status of TCDD-exposed monkeys was evaluated. For TCDD-exposed and unexposed animals, TCDD exposure correlated with an increased serum TCDD concentration. Furthermore, TCDD exposure and an elevated serum TCDD concentration were associated with increased serum levels of triglycerides, 1,2,3,6,7,8-hexachlorodibenzofuran (HxCDF), PCB77, and PCB126. Importantly, the animals with elevated serum levels of PCB77 and PCB126 and increased total serum TCDD equivalents (TEQs) had a high prevalence of endometriosis, and the severity of disease correlated with the serum concentration of PCB77. In immune studies, TCDD exposure correlated with increased tumor necrosis factor alpha (TNFalpha) production by peripheral blood mononuclear cells (PBMC) in response to stimulation by T cell mitogen and decreased NK cytolytic activity. Elevated serum concentrations of TCDD, 1,2,3,6,7,8-HxCDF, and PCB126 correlated with increased numbers of CD3+/CD25- and CD3-/CD25+ leukocytes and enhanced secretion of TNFalpha by mitogen-stimulated PBMC. This evidence suggests that TCDD exposure and endometriosis in the rhesus monkey may be associated with increased serum concentrations of specific coplanar PCB compounds and long-term alterations in systemic immunity. Furthermore, the data suggest a potential involvement of an increased body burden of PCB compounds in the etiology of endometriosis in the rhesus. Recent advances in the detection and assay of individual PHAH congeners in biological samples have made it possible to assess total PHAH body burden in humans and animals. Future studies are expected to exploit this advance to assess the health impact of PHAH body burdens in both exposed individuals and the general population. Serum PHAH concentrations and TEQs in TCDD-exposed monkeys with endometriosis are similar to or lower than blood levels in the general human population; thus, it is important to consider the implications of these findings for human health and the prevalence of endometriosis in humans. Additional studies are warranted, particularly in human subjects, to explore the potential implications of these data.
MeSH term(s)	Animals ; Disease Models, Animal ; Endometriosis/chemically induced ; Endometriosis/immunology ; Endometriosis/physiopathology ; Environmental Exposure ; Environmental Pollutants/toxicity ; Female ; Humans ; Hydrocarbons, Chlorinated/toxicity ; Macaca ; Mice
Chemical Substances	Environmental Pollutants ; Hydrocarbons, Chlorinated
Language	English
Publishing date	2002-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	211003-9
ISSN	1749-6632 ; 0077-8923
ISSN (online)	1749-6632
ISSN	0077-8923
DOI	10.1111/j.1749-6632.2002.tb02781.x
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Article: Environmental dioxins and endometriosis.

Rier, Sherry / Foster, Warren G

Seminars in reproductive medicine

2003 Volume 21, Issue 2, Page(s) 145–154

Abstract: Endometriosis is a common gynecologic problem of unknown etiology. Estrogen dependence and immune modulation are established features of this disease, and environmental contaminants have been suggested to play a role in the pathobiology of this disease ... ...

Abstract	Endometriosis is a common gynecologic problem of unknown etiology. Estrogen dependence and immune modulation are established features of this disease, and environmental contaminants have been suggested to play a role in the pathobiology of this disease as well. Previous work in nonhuman primates has shown that exposure to the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with an increased prevalence and severity of endometriosis. Further animal experiments have implicated dioxin and dioxin-like compounds in this disease. Rodent studies support the plausibility of a role of environmental contaminants in the pathophysiology of endometriosis, although a convincing mechanistic hypothesis has yet to be advanced. Small hospital-based case-control studies have failed to provide compelling evidence for or against an association of environmental contaminants and endometriosis. Herein we review evidence that dioxin and dioxin-like compounds are potent modulators of immune and endocrine function critical to the pathobiology of endometriosis. Furthermore, perspectives on the potential mechanism(s) of dioxin and dioxin-like compound-induced toxicity in endometriosis, important knowledge needs, potential animal models for endometriosis studies, and considerations integral to future human case-control studies are discussed.
MeSH term(s)	Animals ; Dioxins/adverse effects ; Endometriosis/chemically induced ; Environmental Exposure ; Female ; Humans ; Polychlorinated Biphenyls/adverse effects ; Polychlorinated Dibenzodioxins/adverse effects
Chemical Substances	Dioxins ; Polychlorinated Dibenzodioxins ; Polychlorinated Biphenyls (DFC2HB4I0K)
Language	English
Publishing date	2003-05
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2042479-6
ISSN	1526-4564 ; 1526-8004
ISSN (online)	1526-4564
ISSN	1526-8004
DOI	10.1055/s-2003-41321
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Article: Environmental dioxins and endometriosis.

Rier, Sherry / Foster, Warren G

Toxicological sciences : an official journal of the Society of Toxicology

2002 Volume 70, Issue 2, Page(s) 161–170

Abstract: Endometriosis is a common gynecologic problem of unknown etiology. Estrogen dependence and immune modulation are established features of this disease and recently environmental contaminants have been suggested to play a role in the pathobiology of ... ...

Abstract	Endometriosis is a common gynecologic problem of unknown etiology. Estrogen dependence and immune modulation are established features of this disease and recently environmental contaminants have been suggested to play a role in the pathobiology of endometriosis as well. Previous work in nonhuman primates has shown that exposure to the dioxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is associated with an increased prevalence and severity of endometriosis. Further animal experiments have implicated dioxin and dioxin-like compounds in this disease. Rodent studies support the plausibility for a role of environmental contaminants in the pathophysiology of endometriosis although a convincing mechanistic hypothesis has yet to be advanced. Small hospital-based case-control studies have failed to provide compelling evidence for or against an association of environmental contaminants and endometriosis. Herein we review the available literature that provides evidence that dioxin and dioxin-like compounds are potent modulators of immune and endocrine function critical to the pathobiology of endometriosis. Furthermore, perspectives on the potential mechanism(s) of dioxin and dioxin-like compound-induced toxicity in endometriosis, important knowledge needs, potential animal models for endometriosis studies, and considerations integral to future human case-control studies are discussed.
MeSH term(s)	Animals ; Body Burden ; Dioxins/pharmacokinetics ; Dioxins/toxicity ; Disease Models, Animal ; Endometriosis/chemically induced ; Environmental Pollutants/pharmacokinetics ; Environmental Pollutants/toxicity ; Female ; Humans
Chemical Substances	Dioxins ; Environmental Pollutants
Language	English
Publishing date	2002-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1420885-4
ISSN	1096-0929 ; 1096-6080
ISSN (online)	1096-0929
ISSN	1096-6080
DOI	10.1093/toxsci/70.2.161
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Article: Environmental Dioxins and Endometriosis

Rier, Sherry / Foster, Warren G.

Seminars in Reproductive Medicine

2003 Volume 21, Issue 02, Page(s) 145–154

Abstract	Endometriosis is a common gynecologic problem of unknown etiology. Estrogen dependence and immune modulation are established features of this disease, and environmental contaminants have been suggested to play a role in the pathobiology of this disease as well. Previous work in nonhuman primates has shown that exposure to the dioxin 2,3,7,8-tetrachlorodibenzo- P-dioxin (TCDD) is associated with an increased prevalence and severity of endometriosis. Further animal experiments have implicated dioxin and dioxin-like compounds in this disease. Rodent studies support the plausibility of a role of environmental contaminants in the pathophysiology of endometriosis, although a convincing mechanistic hypothesis has yet to be advanced. Small hospital-based case-control studies have failed to provide compelling evidence for or against an association of environmental contaminants and endometriosis. Herein we review evidence that dioxin and dioxin-like compounds are potent modulators of immune and endocrine function critical to the pathobiology of endometriosis. Furthermore, perspectives on the potential mechanism(s) of dioxin and dioxin-like compound;ndinduced toxicity in endometriosis, important knowledge needs, potential animal models for endometriosis studies, and considerations integral to future human case-control studies are discussed.
Keywords	endometriosis ; environmental dioxins ; TCDD ; dioxin-like polychlorinated biphenyls
Language	English
Publishing date	2003-01-01
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	2042479-6
ISSN	1526-4564 ; 1526-8004
ISSN (online)	1526-4564
ISSN	1526-8004
DOI	10.1055/s-2003-41321
Database	Thieme publisher's database

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Article: Immune Aspects of Endometriosis: Relevance of the Uterine Mucosal Immune System

Rier, Sherry E. / Yeaman, Grant R.

Seminars in Reproductive Endocrinology

1997 Volume 15, Issue 03, Page(s) 209–220

Abstract: Endometriosis is classically defined as the growth of endometrial cells at sites outside the uterus. It is a common disease characterized by infertility, chronic pain and adhesion formation. Immune dysregulation, evidenced by decreased clearance of ... ...

Abstract	Endometriosis is classically defined as the growth of endometrial cells at sites outside the uterus. It is a common disease characterized by infertility, chronic pain and adhesion formation. Immune dysregulation, evidenced by decreased clearance of endometrial cells and aberrant production of cytokines by peritoneal fluid leukocytes, has been proposed as a mechanism which allows implantation and growth of ectopic endometrium. Cytokines are primary components of intercellular signaling between uterine epithelial and stromal cells, leukocytes, and the developing conceptus. Because their production is regulated by sex hormones, cytokines are well-placed to play a key role in the extensive tissue remodeling required to accommodate menstruation, implantation and pregnancy. Understanding this specialized hormonally-responsive mucosal immune system within the uterus will be critical to understanding the potential importance of the immune system in the pathogenesis of endometriosis. In this review, highlights of studies describing leukocyte populations, cytokines and cytokine receptors in uterine and ectopic endometrium and their proposed role in the regulation of immune processes and endometrial growth are presented, followed by a review of current data on immune aspects of endometriosis. Studies directed at investigating the hormonal regulation of cytokine secretion by uterine and peritoneal cell populations, and the effect of cytokines on endometrial proliferation, should provide a more complete understanding of their potential role in normal uterine growth and in the pathogenesis of endometriosis.
Keywords	Endometriosis ; endometrium ; leukocytes ; cytokines ; interleukin ; interferon ; tumor necrosis factor ; transforming growth factor ; receptors ; immune system
Language	English
Publishing date	1997-08-01
Publishing place	Stuttgart ; New York
Document type	Article
ZDB-ID	2042479-6
ISSN	1526-4564 ; 0734-8630 ; 1526-8004
ISSN (online)	1526-4564
ISSN	0734-8630 ; 1526-8004
DOI	10.1055/s-2008-1068750
Database	Thieme publisher's database

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Article: The Potential Role of Environmental Toxins in the Pathophysiology of Endometriosis

Bruner-Tran, Kaylon L. / Rier, Sherry E. / Eisenberg, Esther / Osteen, Kevin G.

Gynecologic and Obstetric Investigation

1999 Volume 48, Issue 1, Page(s) 45–56

Abstract: Environmental contaminants that are known to disrupt steroid action can influence the development of reproductive diseases. Our group has focused on whether 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin) can disrupt steroid regulation of ... ...

Institution	Women’s Reproductive Health Research Center, Vanderbilt University School of Medicine, Nashville, Tenn., USA
Abstract	Environmental contaminants that are known to disrupt steroid action can influence the development of reproductive diseases. Our group has focused on whether 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD or dioxin) can disrupt steroid regulation of endometrial matrix metalloproteinase (MMP) expression. The MMPs regulate extracellular matrix turnover in normal tissues, but the inappropriate expression of these enzymes is associated with numerous disease states that involve invasive processes. We have previously shown that secretion of MMPs by human endometrium is critical for establishment of ectopic lesions in a nude mouse model of experimental endometriosis. In this report, we show that TCDD exposure promotes establishment of experimental endometriosis by interfering with the ability of progesterone to suppress endometrial MMP expression.
Keywords	Progesterone ; MMPs ; TGF-β ; TCDD ; PCBs ; Endometriosis
Language	English
Publishing date	1999-11-02
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Session 3: Review
ZDB-ID	800003-7
ISBN	978-3-8055-6987-3 ; 978-3-318-00520-2 ; 3-8055-6987-4 ; 3-318-00520-7
ISSN	1423-002X ; 0378-7346
ISSN (online)	1423-002X
ISSN	0378-7346
DOI	10.1159/000052868
Database	Karger publisher's database

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Journal: Immunoresponsiveness in Endometriosis: Implications of Estrogenic Toxicants

Rier, Sherry E. / Martin, Dan C. / Bowman, Robert E. / Becker, Jeanne L.

EHP (Environmental Health Perspectives) Supplements

1995 Volume 103, Page(s) 151–156

Abstract: Endometriosis is a reproductive disease characterized by the growth of endometrial cells at sites outside the uterus. This disease is a serious disorder associated with chronic pain and infertility, which may be present in 6 million women in this country. ...

Abstract	Endometriosis is a reproductive disease characterized by the growth of endometrial cells at sites outside the uterus. This disease is a serious disorder associated with chronic pain and infertility, which may be present in 6 million women in this country. Traditional medical therapy has consisted of hormonal regimens that limit the action of endogenous estrogen. The etiology of endometriosis is unknown, but studies suggest that soluble factors known as cytokines play a role in disease pathogenesis. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD or dioxin) is an environmental toxicant that alters the action of estrogen in reproductive organs and adversely affects immunocompetence. The incidence of endometriosis was determined in rhesus monkeys that were chronically exposed to dioxin for a period of approximately 4 years. Ten years after termination of dioxin treatment, the presence and severity of endometriosis was assessed by surgical laparoscopy. The incidence of endometriosis correlated with dioxin exposure and disease severity was dependent upon the dose administered. Moderate to severe endometriosis was not found in control animals but was documented in three ot seven animals exposed to 5 ppt dioxin (43 percent) and in five of seven animals exposed to 25 ppt dioxin (71 percent). The frequency of spontaneous disease in the control group was 33 percent, similar to an overall prevalence of 30 percent in 304 rhesus monkeys with no history of dioxin exposure. This study indicates that endometriosis may be associated with dioxin exposure in the rhesus. In view of overwhelming evidence that cytokines participate in the mediation of reproductive-endocrine phenomena and regulation of endometrial growth, future assessment of the effects of environmental toxicants on reproductive health may depend upon our understanding of the bidirectional cytokine network between the immune and endocrine systems.
Keywords	Toxische Substanz ; Immunsystem ; Krankheit ; Mensch ; Zelle ; 2,3,7,8-Tetrachlordibenzo-p-Dioxin ; Steroid ; Hormon ; Biologische Wirkung ; Schadstoffwirkung ; In-Vitro ; In-Vivo ; Exposition ; Schadstoffexposition ; Leukozyten ; Tierversuch ; Affe ; Fuetterungsversuch ; Geschlecht ; Statistische Auswertung ; Fruchtbarkeit
Language	English
Document type	Journal
Database	OPAC and Environmental database (ULIDAT) of The Federal Environment Agency (UBA)

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