Estrogen may play a pivotal role in improving myocarditis by modulating macrophage activation and T-cell responses in a sex-dependent manner.
May modulate myocarditis inflammation by cycle phase in females; hypothesis-generating, requires human studies before clinical consideration.
Autoimmune diseases are more prevalent in women, which has been attributed to the immune stimulatory effects of estrogen (E2). Female mice with myocarditis showed significantly lower amounts of inflammatory cells in the estrus phase than in the diestrus. CD4 cells and activated T-cells were decreased in the estrus phase, while the amount of regulatory T-cells was increased, suggesting a pivotal role of E2 in the improvement of myocarditis. mIR are known to positively/negatively influence Inflammation in a sex-dependent-manner. We propose sex-differences in macrophage-differentiation/activation in chronic myocarditis. Macrophage-activation is regulated be sex-differences in the expression of miR in the heart of myocarditis animals. Male/female mice were infected with COXV3. After 28 days, 9 miRs involved in inflammation or E2 signaling were analyzed by qRT-PCR and immunoblotting. Murine male and female bone marrow macrophages were differentiated into M1 macrophages or into M2 macrophages for 3 days. M1/M2 macrophages were treated with E2 or E2 + ICI for 24 h. Differentiation and gene expression were examined.
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Arellano et al. (2017) studied Myocarditis. Estrogen (E2) / Estrus phase vs. Diestrus phase / untreated was evaluated on Amount of inflammatory cells, CD4 cells, activated T-cells, and regulatory T-cells.
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