Estrogen inhibits lipopolysaccharide-induced tumor necrosis
factor-alpha release from murine macrophages

Zhang, X; Wang, L; Zhang, H; Guo, Dongming; Zhou, Qiao; Qiao, Jingting

doi:10.1358/mf.2001.23.4.634640

Cited by 29 publications

(11 citation statements)

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“…Estrogens are known to suppress monocyte-macrophage recruitment by downregulating CCL2 expression during inflammation and inhibiting TLR4-mediated NFkb activation in macrophages via suppression of micro-RNAs, such as let7a and miR-125b (44,45). Similarly, treating gonadectomized mice with estrogen reduced the levels of TNF and CCL2 and, thus, protected them from influenza virus infection (29,30).…”

Section: Discussionmentioning

confidence: 99%

Sex-Based Differences in Susceptibility to Severe Acute Respiratory Syndrome Coronavirus Infection

Channappanavar

Fett

Mack

et al. 2017

The Journal of Immunology

853

816

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Pathogenic human coronaviruses such as the severe acute respiratory syndrome coronavirus (SARS-CoV) and the Middle East respiratory syndrome coronavirus (MERS-CoV) cause acute respiratory illness. Epidemiological data from the 2002-2003 SARS epidemic and recent MERS indicate that there may be sex-dependent differences in disease outcomes. To investigate these differences, we infected male and female mice of different age groups with SARS-CoV and analyzed their susceptibility to the infection. Our results showed that male mice were more susceptible to SARS-CoV infection compared to age matched females. The degree of sex-bias to SARS-CoV infection increased with advancing age such that middle-aged mice showed much more pronounced differences compared to young mice. Enhanced susceptibility of male mice to SARS-CoV was associated with elevated virus titers, enhanced vascular leakage and alveolar edema. These changes were accompanied by increased accumulation of inflammatory monocyte macrophages (IMMs) and neutrophils in the lungs of male mice and depletion of IMMs partially protected these mice from lethal SARS. Moreover, the sex-specific differences were independent of T and B cell responses. Furthermore, ovariectomy or treating female mice with an estrogen receptor antagonist increased mortality indicating a protective effect for estrogen receptor signaling in mice infected with SARS-CoV. Together, these data suggest that sex differences in susceptibility to SARS-CoV in mice parallel those observed in patients and also identify estrogen receptor signaling as critical for protection in females.

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Section: Discussionmentioning

confidence: 99%

Sex-Based Differences in Susceptibility to Severe Acute Respiratory Syndrome Coronavirus Infection

Channappanavar

Fett

Mack

et al. 2017

The Journal of Immunology

853

816

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show abstract

“…In secondary analyses, the possibility that menopausal status moderates the magnitude of inflammatory responses in women was also explored. To date, no studies have examined this possibility despite evidence that (1) immune cells have receptors for estrogen and progesterone (Turgeon et al, 2006), (2) in vitro treatment of immune cells with estrogen and progesterone modulates pro-inflammatory cytokine production (Rogers & Eastell, 2001; Turgeon et al, 2006; Zhang et al, 2001), and (3) risk for inflammatory disease increases following menopause when levels of these hormones are reduced (Moxley et al, 2002; Turgeon et al, 2006). …”

Section: Introductionmentioning

confidence: 99%

Gender differences in stimulated cytokine production following acute psychological stress

Prather

Carroll

Fury

et al. 2009

Brain, Behavior, and Immunity

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Emerging evidence suggests that acute psychological stress modulates inflammatory competence; however, not all findings are consistent. Gender is one factor that may impact magnitude of response. To explore this possibility, we examined the effects of acute mental stress on lipopolysaccharideinduced production of pro-inflammatory cytokines interleukin (IL)-1 β, IL-6, and tumor necrosis factor (TNF)-α among a relatively healthy sample of midlife men (n=28) and women (n=34). Blood samples for the assessment of cytokine production were drawn before, immediately after and 30 minutes following subjects' performance of an evaluative speech task. Relative to baseline evaluations, the speech stressor elicited a significant increase in stimulated production of all 3 proinflammatory cytokines, as measured 30 minutes following the end of the task. There were no gender differences in the magnitude of this effect. However, men showed a significant decrease in cytokine production from before to immediately following the stressor, whereas women showed no change across this period. Menopausal status partially accounted for these gender differences, with postmenopausal women displaying greater increases in IL-6 and TNF-α production from baselineto-post task when compared to men. These data provide further evidence that acute psychological stress primes the immune system to mount larger inflammatory responses and initial support for gender differences in the patterning of stress-related cytokine activity. In addition, this study presents novel evidence that post-menopausal women may be particularly susceptible to stress-related inflammatory responses. The possibility that this contributes to the increased risk of inflammatory disease observed among older women warrants investigation.

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“…One of the steroid hormones, 17-estradiol (E2) regulates the production of cytokines, antibodies and chemokines. 1) E2 regulates the interleukin-1 (IL-1) promoter activity or tumor necrosis factor-(TNF-) production by macrophages, 2,3) and mediates monocyte chemoattractant protein-1 production by dendritic cells. 4) We have also reported that E2 mediates IgM production by mouse splenocytes through direct cellcell interaction.…”

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confidence: 99%

Effect of Estrogens on the Interferon-γ Producing Cell Population of Mouse Splenocytes

Nakaya

Tachibana

Yamada

2006

Bioscience, Biotechnology, and Biochemistry

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We examined the effect of 17beta-estradiol (E2) on the cytokine production by mouse splenocytes. The production of interferon-gamma (IFN-gamma) was enhanced by E2 stimulation. E2 increased the number of cells expressing IFN-gamma and the IFN-gamma mRNA expression level in the cells. There were low- and high-level cells expressing IFN-gamma in the population. The natural killer (NK) cells and NKT cells were the low-level cells expressing IFN-gamma, and the number of these cells was increased by E2 stimulation. In addition, it was suggested that the enhancing effect of IFN-gamma production by E2 was mediated through estrogen receptor (ER) alpha, and ERbeta agonist stimulated IFN-gamma production. ERs are expressed on plasma membrane as well as in nucleus. The ligand specific to plasma membrane-associated ER (mER) enhanced the IFN-gamma production. In conclusion, our results indicated that E2 up-regulated the IFN-gamma production by mediating ERalpha, ERbeta and mERs.

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Estrogen inhibits lipopolysaccharide-induced tumor necrosis factor-alpha release from murine macrophages

Cited by 29 publications

References 0 publications

Sex-Based Differences in Susceptibility to Severe Acute Respiratory Syndrome Coronavirus Infection

Sex-Based Differences in Susceptibility to Severe Acute Respiratory Syndrome Coronavirus Infection

Gender differences in stimulated cytokine production following acute psychological stress

Effect of Estrogens on the Interferon-γ Producing Cell Population of Mouse Splenocytes

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