The effect of 17β-estradiol on production of cytokines in cultures of peripheral blood

Rogers, Angela; Eastell, Richard

doi:10.1016/s8756-3282(01)00468-9

Cited by 133 publications

(83 citation statements)

References 9 publications

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“…37 Confirmation of the effect of estrogen on cytokine production is noteworthy as hormone-replacement therapy decreases the production of pro-osteoclastogenic cytokines in postmenopausal women. 39 One of the key mechanisms through which estrogen deficiency induces proliferation and increases the life span of bone marrow T cells is the increase in antigen presentation by macrophages and dendritic cells, 36 thanks to a greater expression of Class II TransActivator (CIITA), a transcriptional co-activator acting on the major histocompatibility complex class II promoter, with the final effect of upregulation of major histocompatibility complex class II on macrophages. 23,36 These data have been generated in mouse models.…”

Section: Inflammatory Diseases Immune System and Bonementioning

confidence: 99%

Osteoimmunology: from mice to humans

Sassi¹

2016

Bonekey Reports

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The immune system has been recognized as one of the most important regulators of bone turnover and its deregulation is implicated in several bone diseases such as postmenopausal osteoporosis and inflammatory bone loss; recently it has been suggested that the gut microbiota may influence bone turnover by modulation of the immune system. The study of the relationship between the immune system and bone metabolism is generally indicated under the term 'osteoimmunology'. The vast majority of these studies have been performed in animal models; however, several data have been confirmed in humans as well: this review summarizes recent data on the relationship between the immune system and bone with particular regard to the data confirmed in humans.

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Section: Inflammatory Diseases Immune System and Bonementioning

confidence: 99%

Osteoimmunology: from mice to humans

Sassi¹

2016

Bonekey Reports

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“…With respect to cytokine expression, estrogen in the high concentrations seen in pregnancy can inhibit proinflammatory pathways which include those activated by IL-1β (Polan et al, 1989), IL-6 (Keck et al, 1998, Kikuchi et al, 2000, IL-8 (Rodriguez et al, 2002) and TNF-α (Rogers and Eastell, 2001) as well as inhibiting the activity of natural killer cells (Seaman and Gindhart, 1979). In contrast, the secretion of 'anti-inflammatory interleukins' IL-4 (Kamada et al, 2001), IL-10 (Kanda and Tamaki, 1999) and transforming growth factor (TGF)-β (Hatthachote and Gillespie, 1999) are stimulated by estrogen in these high levels.…”

Section: Page 13 Of 24mentioning

confidence: 99%

Endocrine immune interactions in human parturition

Golightly

Jabbour

Norman

2011

Molecular and Cellular Endocrinology

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Human parturition is an inflammatory event, modulated and influenced by a host of other environmental and physiological processes, including the endocrine hormones.Complex bidirectional communication occurs between the two systems to bring about some of the changes that are seen in labour, an event that is not yet fully understood.Preterm birth is a major problem in obstetrics and neonatology, with dysfunctional labour or prolonged pregnancy also making increasingly significant contributions to maternal morbidity. With better understanding of normal and abnormal parturition we may be able to develop novel ways of treating these complications of pregnancy and reduce maternal and neonatal morbidity and mortality. This review discusses the crucial role that endocrine-immune interaction plays in the process of labour and in the processes of abnormal and preterm labour. We propose that amongst these complex interactions it is the immune system that is the driving force behind human parturition. Keywords Parturition Endocrine InflammationImmune

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“…In this type of osteoporosis, it is known that osteoclastic bone resorption and osteoblastic bone formation are both activated during the early stage of the disease [1,2]. Although the mechanisms underlying the activation of bone resorption are relatively well understood [1][2][3][4][5][6][7], the mechanisms underlying the increase in osteoblastic activity remain unclear.…”

Section: Discussionmentioning

confidence: 99%

“…Subsequently, bone resorption becomes relatively dominant, resulting in the deterioration of bone structure [1,2]. Accumulating evidence suggests that estrogen deficiency induces bone resorption by increasing levels of proinflammatory cytokines such as IL-1, IL-6, TNF-α and HIF1α which enhance the formation and activation of osteoclasts [3][4][5][6][7]. However, Jilka et al [8] reported that the lack of estrogen not only stimulates the formation of osteoclasts but also inappropriately stimulates the formation of osteoblasts in mice.…”

Section: Introductionmentioning

confidence: 99%

Possible Involvement of Leptin in the Elevated Osteoblastic Activity Observed in High Turnover Type Osteoporosis of Ovariectomized Mice

Tezuka¹

2014

J Autacoids

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Postmenopausal osteoporosis is a high turnover type of osteoporosis induced by estrogen deficiency following menopause. In this type of osteoporosis, the osteoblastic activity is known to be elevated even though bone resorption by osteoclasts eventually exceeds bone formation by osteoblasts, resulting in the deterioration of the bone structure. Although the mechanisms underlying the progression of bone resorption in this disease are relatively well understood, the mechanisms underlying the elevated osteoblastic activity are yet to be elucidated. The purpose of this study is to investigate the possibility that leptin, a 16 kDa circulating hormone secreted mainly by white adipose tissue, is involved in the development and/or progression of the high turnover type of osteoporosis. Immunohistochemical analysis and ELISA were used to examine the expression of leptin in bones of ovariectomized mice. To investigate the effect of leptin on proliferation and osteoblastic differentiation of bone marrow stromal cells, cell proliferation assay and real-time RT-PCR analysis were performed using a mouse bone marrow stromal cell line, MMSC3. Immunohistochemistry and ELISA revealed enhanced expression of leptin in bone marrows of ovariectomized mice. A cell proliferation assay detected no significant effect of leptin on the proliferation of MMSC3 cells. In contrast, real-time RT-PCR revealed that leptin promoted the osteoblastic differentiation of this cell line. Estrogen depletion caused by ovariectomy induces the upregulation of leptin expression in the bone marrow cavity, which leads to the elevated osteoblastic activity observed in the early phase of high turnover type osteoporosis of ovariectomized mice.

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The effect of 17β-estradiol on production of cytokines in cultures of peripheral blood

Cited by 133 publications

References 9 publications

Osteoimmunology: from mice to humans

Osteoimmunology: from mice to humans

Endocrine immune interactions in human parturition

Possible Involvement of Leptin in the Elevated Osteoblastic Activity Observed in High Turnover Type Osteoporosis of Ovariectomized Mice

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