Estrogen modulates β2-adrenoceptor-induced cell-mediated and inflammatory immune responses through ER-α involving distinct intracellular signaling pathways, antioxidant enzymes, and nitric oxide

Priyanka, Hannah P.; Singh, Ran Vijay; Pratap, Uday P.; ThyagaRajan, Srinivasan

doi:10.1016/j.cellimm.2014.08.001

Cited by 17 publications

(29 citation statements)

References 44 publications

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“…IFN-γ levels and its mRNA expression were found to be augmented in mouse splenocytes with estrogen stimulation [41]. Similar alterations were found in splenic lymphocytes where estrogen differentially altered lymphoproliferation and cytokine production influenced by estrogen receptors in vitro and in vivo [3,28,42].…”

Section: Discussionsupporting

confidence: 56%

Estrogen upregulates inflammatory signals through NF-κB, IFN-γ, and nitric oxide via Akt/mTOR pathway in the lymph node lymphocytes of middle-aged female rats

Pratap

Sharma

Mohanty

et al. 2015

International Immunopharmacology

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Section: Discussionsupporting

confidence: 56%

Estrogen upregulates inflammatory signals through NF-κB, IFN-γ, and nitric oxide via Akt/mTOR pathway in the lymph node lymphocytes of middle-aged female rats

Pratap

Sharma

Mohanty

et al. 2015

International Immunopharmacology

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“…The increase level of ROS also explained hyperuricemia parallel with the decrease of estrogen levels. [22] Estrogens have systemic antioxidant effects, [23,24] and the protective effects on bones, especially E2, are deficient in menopausal status. [25] …”

Section: Discussionmentioning

confidence: 99%

Gout increases risk of fracture

et al. 2016

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There is still debate on whether high uric acid increases bone mineral density (BMD) against osteoporotic fracture or bone resorption caused by gout inflammation. This study aimed to evaluate whether gout offers a protective effect on bone health or not. We conducted a nationwide population-based retrospective cohort study to evaluate the association between gout history and risk factors of fracture.A retrospective cohort study was designed using the claim data from Longitudinal Health Insurance Database (LHID). A total of 43,647 subjects with gout and a cohort of 87,294 comparison subjects without gout were matched in terms of age and sex between 2001 and 2009, and the data were followed until December 31, 2011. The primary outcome of the study was the fracture incidence, and the impacts of gout on fracture risks were analyzed using the Cox proportional hazards model.After an 11-year follow-up period, 6992 and 11,412 incidents of fracture were reported in gout and comparison cohorts, respectively. The overall incidence rate of fracture in individuals with gout was nearly 23%, which was higher than that in individuals without gout (252 vs 205 per 10,000 person-years) at an adjusted hazard ratio of 1.17 (95% confidence interval = 1.14–1.21). Age, sex, and fracture-associated comorbidities were adjusted accordingly. As for fracture locations, patients with gout were found at significant higher fracture risks for upper/lower limbs and spine fractures. In gout patient, the user of allopurinol or benzbromarone has significantly lower risk of facture than nonusers.Gout history is considered as a risk factor for fractures, particularly in female individuals and fracture sites located at the spine or upper/lower limbs.

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“…For women after menopause estrogen levels drop dramatically. Among the many roles attributed to this hormone is an immunomodulatory role, its decline would favor a proinflammatory state as women age [117]. Estrogen also has effects on monopoyesis, which may be involved in thrombotic events [118,119].…”

Section: Hormonal Changesmentioning

confidence: 99%