Hormonal modulation of Toxoplasma gondii infection: Regulation of hormonal receptors and cytokine production in THP-1 cells

Galván-Ramírez, María de la Luz; Arellano, Adrián Ramírez De; Rodríguez-Pérez, Laura Rocío; Lopez-Pulido, Edgar I.; Muñoz‐Valle, José Francisco; Pereira‐Suárez, Ana Laura

doi:10.1016/j.exppara.2019.107721

Cited by 11 publications

(19 citation statements)

References 25 publications

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“…However, it was observed that E2 treated HPBMs of men did not show increased production of this cytokine; and the IL-12 gene expression in these cells was lower compared to untreated HPBMs. Contrary to our observations, Galvań-Ramıŕez et al (2019) demonstrated that THP-1 monocytes, pre-treated with E2, and subsequently stimulated with T. gondii cells, exhibit downregulation of IL-12. However, their study differed in terms of the pre-treatment duration, with pre-treatment lasting for 48 h in Galvań-Ramıŕez et al (2019), whereas in our study, pre-treatment lasted for 24 h. In a study with LPS-stimulated whole blood culture, it was observed that during the pre-ovulatory phase, estradiol significantly increased the levels of IL-12 production, while E2 significantly decreased IL-12 levels during pregnancy (Matalka, 2003).…”

Section: Discussioncontrasting

confidence: 99%

“…However, treatment with either E2 or PG alone did not induce upregulation of IL-10. Galvań-Ramıŕez et al (2019) reported that THP-1 monocytes, stimulated with Toxoplasma gondii and treated with E2 showed increased production of IL-10; however, no differences were observed when pre-treated with progesterone. Secretion of IL-10 was suppressed by E2 in a dose-dependent manner in NR8383 macrophages (Kou et al, 2015).…”

Section: Discussionmentioning

confidence: 98%

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Effects of 17β-Estradiol on Monocyte/Macrophage Response to Staphylococcus aureus: An In Vitro Study

Souza

Barbosa

Coelho

et al. 2021

Front. Cell. Infect. Microbiol.

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To describe how 17β-estradiol (E2) influence in the monocyte/macrophage response induced by S. aureus in in vitro models of murine peritoneal macrophages (MPMs) and human peripheral blood monocytes (HPBM). MPMs (2 x 105/ml) were isolated from sham (n=3) and ovariectomized (OVX) females (n = 3) and males (n = 3) after induction by thioglycolate. The MPMs obtained from OVX females and males were treated for 24 hours with 17β-estradiol (E2) (10-7 M), and after that, inoculation with S. aureus was carried out for 6 hours. The macrophages were collected and destined to evaluate the relative gene expression of TNF-α, IL-1β, IL-6, IL-8 and TLR2. For the in vitro model of HPBMs, six men and six women of childbearing age were selected and HPBMs were isolated from samples of the volunteers’ peripheral blood. In women, blood was collected both during menstruation and in the periovulatory period. HPBMs were inoculated with S. aureus for 6 hours and the supernatant was collected for analysis of cytokines by Luminex and the HPBMs were removed for analysis of 84 genes involved in the host’s response to bacterial infections by RT-PCR array. Previous treatment with E2 decreased the gene expression and production of proinflammatory cytokines, such as TNF-α, IL-1β and IL-6 and decreased the expression of TLR2 tanto em MPMs quanto em HPBMs. The analysis of gene expression shows that E2 inhibited the NFκB pathway. It is suggested that 17β-estradiol acts as an immunoprotective in the monocyte/macrophage response induced by S. aureus.

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionmentioning

confidence: 98%

Effects of 17β-Estradiol on Monocyte/Macrophage Response to Staphylococcus aureus: An In Vitro Study

Souza

Barbosa

Coelho

et al. 2021

Front. Cell. Infect. Microbiol.

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“…Five reasons led us to investigate the role of GPER rather than the nuclear estrogen receptors in the observed effect: (1) naive unstimulated THP-1 cells, as primary human monocytes, do not express ERα66 or ERβ at the protein level, while they express ERα46, ERα36, and GPER (Cutolo et al 2001;Pelekanout et al 2016;Galván-Ramírez et al 2019; in house unpublished data); (2) the RACK1 promoter does not contain a nuclear estrogen receptor element (Del Vecchio et al 2009); ( 3) the effects of 17βestradiol on RACK1 are more evident at higher concentrations than the physiological values, in agreement with a possible involvement of GPER that is typically associated with higher 17β-estradiol concentrations (Prossnitz and Barton 20141); (4) DHEA, the first compound we have identified able to modulate the levels of RACK1 (Corsini et al 1999), has been reported to interact at physiological relevant concentration with GPER with effects mediated in part by AP-1 and AR (Teng et al 20145);…”

Section: Role Of Gper In Estrogen-active Compound-induced Rack1 Expressionmentioning

confidence: 99%

“…However, they do exhibit thymus atrophy, impaired glucose tolerance, and altered bone growth (reviewed in Filardo and Thomas 2012). Unstimulated THP-1 cells, as primary human monocytes, do not express ERα66 or ERβ at the protein level, while they express GPER, and shown the presence of a low-affinity estrogen-receptor activity (Cutolo et al 2001;Pelekanout et al 2016;Galván-Ramírez et al 2019). Membrane-localized ERs rapidly signal through kinase cascades, calcium, and other second messengers (Zimmerman et al 2016;Barton et al 2018).…”

Section: Aq3 Aq4mentioning

confidence: 99%

Effect of estrogen-active compounds on the expression of RACK1 and immunological implications

et al. 2020

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“…Recently our research group demonstrated that T. gondii induces the expression of ERα and ERβ and lowers prolactin receptor (PRLR) in THP-1 monocytes cells. Progesterone decreases PRLR and ERβ and increases ERα; E2 decreases PRLR, and prolactin (PRL) reduces ERα and ERβ expression [ 39 ]. However, the effect of estradiol and progesterone on cultured neurons infected with Toxoplasma is unknown.…”

Section: Introductionmentioning

confidence: 99%

Effect of 17β-Estradiol, Progesterone, and Tamoxifen on Neurons Infected with Toxoplasma gondii In Vitro

et al. 2021

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Toxoplasma gondii (T. gondii) is the causal agent of toxoplasmosis, which produces damage in the central nervous system (CNS). Toxoplasma–CNS interaction is critical for the development of disease symptoms. T. gondii can form cysts in the CNS; however, neurons are more resistant to this infection than astrocytes. The probable mechanism for neuron resistance is a permanent state of neurons in the interface, avoiding the replication of intracellular parasites. Steroids regulate the formation of Toxoplasma cysts in mice brains. 17β-estradiol and progesterone also participate in the control of Toxoplasma infection in glial cells in vitro. The aim of this study was to evaluate the effects of 17β-estradiol, progesterone, and their specific agonists–antagonists on Toxoplasma infection in neurons in vitro. Neurons cultured were pretreated for 48 h with 17β-estradiol or progesterone at 10, 20, 40, 80, or 160 nM/mL or tamoxifen 1 μM/mL plus 17β-estradiol at 10, 20, 40, 80, and 160 nM/mL. In other conditions, the neurons were pretreated during 48 h with 4,4′,4″-(4-propyl-[1H] pyrozole-1,3,5-triyl) trisphenol or 23-bis(4-hydroxyphenyl) propionitrile at 1 nM/mL, and mifepristone 1 µM/mL plus progesterone at 10, 20, 40, 80, and 160 nM/mL. Neurons were infected with 5000 tachyzoites of the T. gondii strain RH. The effect of 17β estradiol, progesterone, their agonists, or antagonists on Toxoplasma infection in neurons was evaluated at 24 and 48 h by immunocytochemistry. T. gondii replication was measured with the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide reduction assay. 17β-Estradiol alone or plus tamoxifen reduced infected neurons (50%) compared to the control at 48 h. Progesterone plus estradiol decreased the number of intracellular parasites at 48 h of treatment compared to the control (p < 0.001). 4,4′,4″-(4-propyl-[1H] pyrozole-1,3,5-triyl) trisphenol and 23-bis(4-hydroxyphenyl) propionitrile reduced infected neurons at 48 h of treatment significantly compared to the control (p < 0.05 and p < 0.001, respectively). The Toxoplasma infection process was decreased by the effect of 17β-estradiol alone or combined with tamoxifen or progesterone in neurons in vitro. These results suggest the essential participation of progesterone and estradiol and their classical receptors in the regulation of T. gondii neuron infection.

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Hormonal modulation of Toxoplasma gondii infection: Regulation of hormonal receptors and cytokine production in THP-1 cells

Cited by 11 publications

References 25 publications

Effects of 17β-Estradiol on Monocyte/Macrophage Response to Staphylococcus aureus: An In Vitro Study

Effects of 17β-Estradiol on Monocyte/Macrophage Response to Staphylococcus aureus: An In Vitro Study

Effect of estrogen-active compounds on the expression of RACK1 and immunological implications

Effect of 17β-Estradiol, Progesterone, and Tamoxifen on Neurons Infected with Toxoplasma gondii In Vitro

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