The effect of estradiol on human myelomonocytic cells. 1. Enhancement of colony formation

Maoz, Helen; Kaiser, Nurit; Halimi, Michele; Barak, Vivian; Haimovitz, Adriana; Weinstein, Daniel C.; Simon, Alexander; Biran, S; Treves, Abraham J.

doi:10.1016/0165-0378(85)90027-0

Cited by 33 publications

(14 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, the number of macrophages was increased during the process of sexual maturity in immature rats [4]. Maoz et al [19] also noted that peripheral blood monocyte counts increased during the periods of high circulating estradiol levels, such as the ovulatory period in healthy women. Regarding IL-1 production, Tabibzadeh and Sun [20] showed cyclic changes in IL-1a gene product in the endometrial epithelium, and suggested that the synthesis and/or secretion of IL-1 may be under the control of systemic steroid signals.…”

Section: Discussionmentioning

confidence: 99%

Changes in Interleukin-1 Production of Peritoneal Macrophages during Estrous Cycle in Golden Hamsters.

et al. 1996

View full text Add to dashboard Cite

Abstract. The present study demonstrated the change in interleukin-1 (IL-1) production of peritoneal macrophages during the estrous cycle in golden hamsters and discussed its possible roles in ovarian function. Macrophages were collected from the peritoneal cavity at 0900 h on various days of the estrous cycle and incubated for 6 h in the presence of ovine pituitary LH (500 ng/ml). The IL-1 concentration in the media was measured by bioassay with the A375S2 human melanoma cell line. The number of macrophages significantly (P<0.01) increased on estrus and proestrus compared with diestrus 1 or diestrus 2. LH-induced production of IL-1 was also greater (P<0.01) on proestrus (292 ± 36 pg/106 cells/ ml) and estrus (222 ± 30 pg/106 cells/ml) than on diestrus 1(34 ± 15 pg/106 cells/ml) or diestrus 2 (117 ± 16 pg/106 cells/ml). To clarify the factor inducing the changes in peritoneal macrophages, hamsters were ovariectomized on diestrus 1, and 3 weeks later the animals were treated with sc injections of progesterone (200.tg/day), testosterone (100 jug/day), estradiol (10 , tg/day) or sesame oil for three days. The hamsters were killed 24 h after the last injection, and the number and IL-1 producing capacity of macrophages were determined. The number of macrophages and their response to LH to produce IL-1 were increased significantly (P<0.01) by estradiol treatment but not by progesterone or testosterone treatment. It was concluded that the peritoneal macrophages became more sensitive to LH to produce IL-1 on proestrus and estrus in cyclic hamsters, and that these changes in macrophages, probably induced by estradiol, would play important roles in ovarian function.

show abstract

Section: Discussionmentioning

confidence: 99%

Changes in Interleukin-1 Production of Peritoneal Macrophages during Estrous Cycle in Golden Hamsters.

et al. 1996

View full text Add to dashboard Cite

show abstract

“…A reduction in the capacity of lymphocytes from estrogen-treated mice to transfer EAE was observed, and is consistent with the hypothesis that estrogen in the lymphoid microenvironment can alter T cell function. Estrogen has been shown to alter the function of various immunocompetent cells including B cells (42,43), T cells (30), macrophages (44,45), NK cells (46), endothelial cells (47,48), and stromal cells (49). Much attention has been focused on the ability of estrogen to regulate T cell cytokine secretion.…”

Section: Discussionmentioning

confidence: 99%

Low-Dose Estrogen Therapy Ameliorates Experimental Autoimmune Encephalomyelitis in Two Different Inbred Mouse Strains

Bebo

Fyfe‐Johnson²,

Adlard³

et al. 2001

The Journal of Immunology

318

286

View full text Add to dashboard Cite

It has been proposed that homeostatic levels of estrogen can enhance female susceptibility to autoimmunity, whereas the heightened levels of estrogen associated with pregnancy are protective. This hypothesis was tested using the mouse model of experimental autoimmune encephalomyelitis (EAE). Diestrus (<100 pg/ml in serum) levels of 17β-estradiol were found to significantly reduce the clinical manifestations of active EAE in both male and female mice. Estriol was also effective but at doses below those previously established for pregnancy. The reduction in disease severity was accompanied by a coincident reduction in the number and size of inflammatory foci in the CNS of estrogen (17β-estradiol or estriol)-treated mice. Recipients of encephalitogenic T cells from low-dose estrogen-treated mice developed less severe paralysis than mice receiving T cells from placebo-treated mice. A modest shift in Th1/Th2 balance suggested that low dose estrogen therapy could bias the immune reaction toward a protective anti-inflammatory cytokine response. However, estrogen treatment at the onset of active EAE failed to reduce disease severity, a result that is consistent with the hypothesis that naive cells are more sensitive to sex hormones than differentiated effector cells. These data suggest that treatment with low doses of estrogen can reduce the capacity of developing myelin-reactive T cells to initiate disease and challenges the idea that increased susceptibility to autoimmunity in females is dependent on homeostatic levels of estrogen.

show abstract

“…Several reports have revealed that estrogens exert immunomodulatory activities both in vivo and in vitro by interacting with several cell lineages involved in the immune response [Maoz et al, 1985;Paavonen et al, 1985;Hu et al, 1988;Cutolo et al, 1995]. In particular, it has been reported that estrogens positively affect IL-1b and TNFa mRNA expression in TPA-stimulated THP-1 cells [Shanker et al, 1994a,b].…”

mentioning

confidence: 96%

Phorbol diester 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) up‐regulates the expression of estrogen receptors in human THP‐1 leukemia cells

Cutolo

Carruba

Villaggio

et al. 2001

J of Cellular Biochemistry

View full text Add to dashboard Cite

In the present work, we have inspected expression of estrogen receptors (ER) and their regulation by the phorbol diester 12-O-tetradecanoylphorbol 13-acetate (TPA) in a leukemic cell line, the THP-1 cells, using multiple experimental approaches. Firstly, ligand binding assay (LBA) revealed that control (unstimulated) THP-1 cells express type I (high affinity, limited capacity) ER in the nuclear fraction only, whilst treatment of cells with TPA resulted in the appearance of type I ER in the soluble fraction as well, with the 50 ng/ml dose and the 48 h incubation time being the most effective experimental condition. A concomitant increase of type II ER was also seen in both soluble and nuclear cell fractions. Unstimulated THP-1 cells were found to be ER negative by immunocytochemistry; conversely, cells exposed to 50 ng/ml TPA for 48 h stained positively for ER, with the majority of cells having a strong nuclear staining. Scrutiny of ER mRNA expression using reverse transcriptase-polymerase chain reaction showed the presence of a wild type ER transcript in both control and TPA-treated THP-1 cells, though levels of ER mRNA were found to be comparatively higher in the latter. This combined evidence would imply that the TPA-induced differentiation of THP-1 cells is accompanied by the rise of high affinity (type I) ER, suggesting that estrogens may play a role in the regulation of macrophage activity during the inflammatory and/or the immune response.

show abstract

The effect of estradiol on human myelomonocytic cells. 1. Enhancement of colony formation

Cited by 33 publications

References 30 publications

Changes in Interleukin-1 Production of Peritoneal Macrophages during Estrous Cycle in Golden Hamsters.

Changes in Interleukin-1 Production of Peritoneal Macrophages during Estrous Cycle in Golden Hamsters.

Low-Dose Estrogen Therapy Ameliorates Experimental Autoimmune Encephalomyelitis in Two Different Inbred Mouse Strains

Phorbol diester 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) up‐regulates the expression of estrogen receptors in human THP‐1 leukemia cells

Contact Info

Product

Resources

About