Oncotarget · 2017 · 22 citations · 20 references
Life SciencesImmunologyPathologyImmunopathologyInflammationInnate ImmunityInflammation In Infectious DiseaseInflammatory Cell SignalingInflammatory SignalingInnate Immune ModulationInnate Immune Signaling PathwaysMastitisAcute Inflammatory ResponseEpithelial Cell NecrosisInflammatory Response GenesMammary Gland ImmunologyMammary Gland InflammationMammary InflammationMicrorna In InflammationMicrorna Regulation Of Inflammation
// Weijing Sun 1, * , Qi Wang 1, * , Yingfang Guo 1, * , Yifan Zhao 1 , Xinying Wang 1 , Zhenbiao Zhang 1 , Ganzhen Deng 1 and Mengyao Guo 1 1 College of Veterinary Medicine, Huazhong Agricultural University, Wuhan 430070, People’s Republic of China * These authors have contributed equally to this work Correspondence to: Mengyao Guo, email: gmy1985@163.com Keywords: selenium, mastitis, S. aureus, miRNA-146, inflammation Received: June 20, 2017 Accepted: August 04, 2017 Published: September 08, 2017 ABSTRACT We studied the effects of selenium (Se) on the inflammatory response in Staphylococcus aureus ( S. aureus )-infected mastitis-model mice and mammary epithelial cells. In infected mice, Se elicited a dose-dependent decrease in mammary gland pathology that included inflammatory cell infiltration, disorganized acinar structure and mammary cell necrosis. Se decreased inflammation by increasing miR-146a and decreasing TLR2/6 as well as NF-κB and MAPK signaling pathways in mammary tissue from infected mice and mammary epithelial cells. A miR-146a inhibitor suppressed the anti-inflammatory effects of Se in infected mammary epithelial cells. Se, miR-146a and TLR2 were associated in determining the inflammatory response in mouse with infection-induced mastitis. Thus, Se inhibits pro-inflammatory responses in mammary tissues from S. aureus -infected mice by inducing miR-146a.
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