Selenium ameliorates Staphylococcus aureus-induced inflammation in bovine mammary epithelial cells by inhibiting activation of TLR2, NF-κB and MAPK signaling pathways

• DOI: 10.1186/s12917-018-1508-y
• Publication Date: 2018-06-20T08:34:42Z
• Authors: Heng Wang; Chongliang Bi; Yinjie Wang; Jun Sun; Xia Meng; Jianji Li
• Keywords: Mammary; 0301 basic medicine; 0303 health sciences; MAP Kinase Signaling System; Veterinary medicine; Blotting, Western; NF-kappa B; Staphylococcal Infections; MAPK; NF-κB; Toll-Like Receptor 2; 3. Good health; Selenium; 03 medical and health sciences; SF600-1100; TLR2; Animals; Cattle; Female; Mastitis, Bovine; Se; Cells, Cultured; Research Article

Staphylococcus aureus (S. aureus) internalization into bovine mammary epithelial cells (bMECs) is considered an important pathogenic mechanism for the establishment of mastitis. Given interesting link between selenium (Se) status and mastitis, our objective was to prove that Se essential suppress pro-inflammatory mediators, in part, by modulation Toll-like receptor2 (TLR2), nuclear factor kappaB (NF-κB) mitogen activated protein kinase (MAPK) signal transduction pathway bMECs.Results showed (0~ 16 μM) did not affect growth bMECs. The mRNA expression TLR2, Myeloid differentiation 88 (Myd88), Interleukin-1 receptor-associated kinase4 (Irak4), kinase1 (Irak1) TNF factor6 (Traf6) TLR2 were increased or significantly S. aureus. played role regulating genes Myd88, Traf6 but controlling Irak4 Irak1. In addition, exerted strong inhibitory effects on tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β) interleukin-6 (IL-6) induced To further investigate possible signaling mechanisms involved processes, we analyzed MAPK NF-κB inflammation response aureus-stimulated bMECs vitro. Results phosphorylation alpha (IκBα), p65, p38 extracellular regulated (Erk) It indicated pathway. We also examined IκBα, Erk pathway, which have well been proved control synthesis release mediators during inflammation. findings are exciting, pretreatment with (4, 8 suppressed Erk.These results suggest down-regulates inflammatory TNF-α, IL-1β IL-6 gene expressions via bMECs, may be responsible anti-inflammatory effect Se.