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Fig. 3 | Reproductive Biology and Endocrinology

Fig. 3

From: Estrogen-sensitive activation of SGK1 induces M2 macrophages with anti-inflammatory properties and a Th2 response at the maternal–fetal interface

Fig. 3

LPS/TLR4 promotes a pro-inflammatory Th1 immune profile, and E2 enhances SGK1 activity through PI3K in LPS-stimulated THP-1 macrophages. A Levels of IL4 and IL-5 (Th2 cytokines), and IFN-γ (Th1 cytokine) in the supernatants of THP-1-derived macrophages treated with or without LPS. B The ratio of IL-4/IFN-γ (Th2/Th1 cytokines) derived from the data in (A). C Cell-free supernatants were collected after 24 h of stimulation with (LPS group) or without (control group) the TLR4 ligand LPS derived from Escherichia coli 0111:B4, and LPS-triggered secretions of pro-inflammatory cytokines IL-12p70, TNF-α, and IL-6 of THP-1-derived macrophages were determined using a ProcartaPlex® Multiplex Immunoassay. D Western blot (left) of whole-cell lysates from LPS-stimulated macrophages pretreated with E2 in the presence and absence of PI3K inhibitor LY294002. Blots were probed with antibodies to t-SGK1, p-SGK1, and total β-actin. Densitometric quantification (right) of the arithmetic mean (SEM) ratio of phospho-to-total proteins for SGK1 in LPS-triggered macrophages pretreated with E2 in the presence and absence of LY294002. Three to six independent samples were analyzed. Data are presented as the arithmetic means ± SEM. ***P < 0.001, contrasted with the control group; ∆∆∆P < 0.001, contrasted with the LPS group; ###P < .001, contrasted with the LPS + E2 group. LPS, lipopolysaccharide; TLR4, Toll-like receptor; Th, T helper; E2, estradiol; SGK1, serum-glucocorticoid regulated kinase; PI3K, phosphoinositide 3-kinase; IL, interleukin; IFN-γ, interferon gamma; TNF, tumor necrosis factor; p-, phospho-; SEM, Standard Error of the Mean

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