id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-327086-u3l8nr73	Mauvais-Jarvis, Franck	Estradiol, Progesterone, Immunomodulation, and COVID-19 Outcomes	2020-07-30		.txt	text/plain	4712	214	34	Abbreviations: COVID-19, coronavirus disease-2019; E2, 17β-estradiol; ER, estrogen receptor; HCC, hepatocellular carcinoma; IL-1β, interleukin-1β; IL-6, interleukin-6; ISARIC, International Severe Acute Respiratory and Emerging Infections Consortium; MERS-CoV, Middle East respiratory syndrome coronavirus; MHT, menopausal hormone therapy; P4, progesterone; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2; SERM, selective estrogen receptor modulator; TNF-α, tumor necrosis factor α; Tregs, regulatory T cells. In most experimental human or rodent models, the anti-inflammatory actions of E2 on innate immunity includes the suppression of the production of proinflammatory cytokines, for example, IL-6, IL-1β, and TNF-α, by monocytes and macrophages (a major factor in the COVID-19 cytokine storm) and a strong inhibition of CCL2, thus preventing innate immune cells migration into inflamed areas, particularly neutrophils and monocytes. Taken together, these findings suggest that E2 and related SERMs have 2 potential protective mechanisms of action against SARS-CoV-mediated pneumonias in mice: 1) an estrogen-dependent decrease in the deadly innate immune response and cytokine storm in the lungs, thus preventing respiratory failure, and 2) specific to SERMs, an off-target direct inhibition of SARS-CoV replication and cytopathic effects.	./cache/cord-327086-u3l8nr73.txt	./txt/cord-327086-u3l8nr73.txt