The Complex Role of Estrogens in Inflammation - 0 views
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These studies suggest inflammation-dependent up-regulation of ERβ relative to ERα.
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up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
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it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
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it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
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In cycling women, the largest quantities of Ig were detected before ovulation
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In contrast, E2 at high concentrations leads to a suppression of B-lymphocyte lineage precursors
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E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
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In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
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Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
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IFN-γ, IL-12, and TNF were allocated to Th1 reactions
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IL-4, IL-5, and IL-10 to Th2 responses
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antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
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no direct effects of estrogens on Th17 cells or IL-17 secretion have been described until now.
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So-called Th17 cells producing IL-17 are the main T cells responsible for chronic inflammation.
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Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
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in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
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In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
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increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
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secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
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The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
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experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
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E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
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It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
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important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
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low E2 concentrations were demonstrated to have no or even stimulatory effects
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This renders a woman in the postmenopausal phase to a more proinflammatory situation
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most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
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E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
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SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis
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Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
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great review of the complex interaction between Estrogens and inflammation. Reference here is in females.
