Abstract
S100A7 has received extensive attention in the prevention and treatment of mastitis across a broad spectrum, yet there is a little information about its mechanism, especially in the immunomodulatory effects of estrogen. In the present study, based on the milk bacteriological culture (BC) of 30 dairy goats, the concentration of both estrogen and S100A7 in the BC-positive samples was not significantly different than in the BC-negative samples; the estrogen abundance in subclinical and clinical mastitis samples also showed only a limited difference; compared with healthy samples, the S100A7 abundance in subclinical mastitis samples differed little, while it was significantly decreased in clinical mastitis samples. Moreover, the relationship between estrogen and S100A7 was positive, and the regression equation was y = 0.3206x + 23.459. The goat mammary epithelial cells (gMECs) were isolated and treated with 1, 10, 100 nM E2 and/or 5 μg/mL lipopolysaccharide (LPS), respectively, for 6 h. Compared with control samples, 5 μg/mL LPS, 10 nM E2 and 100 nM E2 markedly induced S100A7 expression and secretion. More than separated treatment, the cooperation of LPS and E2 also significantly increased S100A7 expression, rather than S100A7 secretion. The p-ERK was up-regulated markedly with 100 nM E2 treatment, while the expression of p-JNK, p-p38 and p-Akt had little effect. The G protein-coupled estrogen receptor 1(GPER1) agonist G1 markedly induced S100A7 expression and secretion in gMECs, and the estrogen nuclear receptor antagonist ICI and GPER1 antagonist G15 significantly repressed this process. In conclusion, E2 binds to nuclear and membrane receptors to regulate the expression and secretion of S100A7 via the ERK1/2-signaling pathway in gMECs.