Ovariectomized mice and postmenopausal women exhibit analogous loss of genital epithelial integrity.

Calla, Nirk E. Quispe; Miguel, Rodolfo D. Vicetti; Aceves, Kristen M; Huang, Huijie; Howitt, Brooke E.; Cherpes, Thomas L.

doi:10.1080/21688370.2020.1865760

Cited by 7 publications

(4 citation statements)

References 42 publications

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“…Hormones were usually delivered via multiple injections or intravaginal administration, occurring over several days prior to infection. The dosage of estradiol used in previous investigations varied from 10ug- 5mg/day depending on the animal species and study ( Rank et al., 1982 ; Pasley et al., 1985 ; de Jonge et al., 2011 ; Quispe Calla et al., 2021 ). Importantly, serum concentrations of estrogen and/or progesterone were often not measured to determine if a physiologically relevant concentration was achieved.…”

Section: Discussionmentioning

confidence: 99%

The hormonal environment and estrogen receptor signaling alters Chlamydia muridarum infection in vivo

Gravitte

Kintner

Brown

et al. 2022

Front. Cell. Infect. Microbiol.

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Genital Chlamydia is the most common bacterial sexually transmitted infection in the United States and worldwide. Previous studies indicate that the progression of chlamydial infection is influenced by various factors, including the female sex hormones estrogen and progesterone. Sex hormone levels naturally fluctuate in women throughout their menstrual cycle. Varying concentrations of estrogen and progesterone may impact the progression of chlamydial infection and the host’s immune response to Chlamydia. Estrogen signals through estrogen receptors (ERs), ERα and ERβ. These receptors are similar in structure and function, but are differentially expressed in tissues throughout the body, including the genital tract and on cells of the immune system. In this study, we used ovariectomized (OVT) BALB/c mice to investigate the impact of long-term administration of physiologically relevant concentrations of estrogen (E2), progesterone (P4), or a combination of E2/P4 on the progression of and immune response to C. muridarum infection. Additionally, we used ERα and ERβ knockout C57/BL6 mice to determine the how ERs affect chlamydial infection and the resulting immune response. Estrogen exposure prevented C. muridarum infection in vaginally infected OVT mice exposed to E2 alone or in combination with P4, while OVT or Sham mice exposed to hormone free, P4 or depo-medroxyprogesterone acetate shed similar amounts of chlamydiae. The hormonal environment also altered T cell recruitment and IFNϵ production the genital tracts of infected OVT and Sham mice on day 10 post infection. The absence of ERα, but not ERβ, in ER knockout mouse strains significantly changed the timing of C. muridarum infection. ERαKO mice shed significantly more chlamydiae at day 3 post infection and resolved the infection faster than WT or ERβKO animals. At day 9 post infection, flow cytometry showed that ERαKO mice had more T cells present and targeted RNA sequencing revealed increased expression of CD4 and FOXP3, suggesting that ERαKO mice had increased numbers of regulatory T cells compared to ERβKO and WT mice. Mock and chlamydia-infected ERαKO mice also expressed more IFNϵ early during infection. Overall, the data from these studies indicate that sex hormones and their receptors, particularly ERα and ERβ, differentially affect C. muridarum infection in murine models of infection.

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Section: Discussionmentioning

confidence: 99%

The hormonal environment and estrogen receptor signaling alters Chlamydia muridarum infection in vivo

Gravitte

Kintner

Brown

et al. 2022

Front. Cell. Infect. Microbiol.

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“…In the context of stroke, the neuroprotective effects of 17β-estradiol have been demonstrated in OVX animal models of ischemic stroke. OVX animals are the widely accepted model for post-menopausal women, as the removal of ovaries in female animals effectively mimics the diminished estrogen levels observed in post-menopausal women ( 128 ). Based on an extensive review of experimental studies, estrogen was found to reduce lesion volume after transient or permanent cerebral ischemic stroke in a dose-dependent manner.…”

Section: Ert: Estrogen and Immune Regulationmentioning

confidence: 99%

Immunomodulatory role of estrogen in ischemic stroke: neuroinflammation and effect of sex

Zhong¹,

Sun²,

Lü³

et al. 2023

Front. Immunol.

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Although estrogen is predominantly related to the maintenance of reproductive functioning in females, it mediates various physiological effects in nearly all tissues, especially the central nervous system. Clinical trials have revealed that estrogen, especially 17β-estradiol, can attenuate cerebral damage caused by an ischemic stroke. One mechanism underlying this effect of 17β-estradiol is by modulating the responses of immune cells, indicating its utility as a novel therapeutic strategy for ischemic stroke. The present review summarizes the effect of sex on ischemic stroke progression, the role of estrogen as an immunomodulator in immune reactions, and the potential clinical value of estrogen replacement therapy. The data presented here will help better understand the immunomodulatory function of estrogen and may provide a basis for its novel therapeutic use in ischemic stroke.

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“…This study utilized bilateral ovariectomized mice to simulate patients undergoing ovariectomy [11]. This study aimed to investigate changes in vaginal morphology and measure the potential effects of VMT.…”

Section: Introductionmentioning

confidence: 99%

Vaginal microbiota transplantation alleviates vaginal atrophy in ovariectomized mice

Xu,

Zhu,

Zou

et al. 2024

Preprint

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Genitourinary menopausal syndrome (GSM) is a prevalent symptom in menopausal women, affecting over 50% of older women and patients with loss of ovarian function. The role of factors other than estrogen, such as the vaginal microbiota, in the development of GSM has not been fully explored. Therefore, we selected 8-week-old C57 mice with bilateral oophorectomy for experimentation. After four weeks of treatment, we observed that the vaginal epithelium of ovariectomized mice showed signs of atrophy, and the structure and metabolites of vaginal microbiota showed significant differences. Vaginal transplantation of microbiota from ovary-intact mice significantly ameliorated the vaginal atrophy of ovariectomized mice and altered the structure and metabolism of vaginal microbiota. These findings indicate that ovarian activity significantly affects the structure and metabolism of vaginal microbiota. The vaginal microbiota of ovary-intact mice may promote vaginal health by upregulating ER (estrogen receptor) in vaginal epithelial cells in ovariectomized mice, which in turn promotes cell proliferation. Further studies are needed to investigate the interactions between vaginal bacterial microbiota and vaginal health. This finding can help develop new therapeutic strategies and interventions for patients suffering from vaginal atrophy.

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Ovariectomized mice and postmenopausal women exhibit analogous loss of genital epithelial integrity.

Cited by 7 publications

References 42 publications

The hormonal environment and estrogen receptor signaling alters Chlamydia muridarum infection in vivo

The hormonal environment and estrogen receptor signaling alters Chlamydia muridarum infection in vivo

Immunomodulatory role of estrogen in ischemic stroke: neuroinflammation and effect of sex

Vaginal microbiota transplantation alleviates vaginal atrophy in ovariectomized mice

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