Mastitis induced by Staphylococcus aureus (S. aureus) is a serious problem which will causes serious economic losses to the bovine industry [1, 2]. Meanwhile due to the ability of S. aureus to internalize into host cell, mastitis induced by S. aureus is often difficult to cure. Along with the intensity and persistence of infection, most animals cannot escape the fate of elimination . Thus finding effective ways to prevent or cure mastitis induced by S. aureus has become research focus on dairy industry.
Innate immunity plays an important role in defensing against pathogens. Once stimulated innate immunity is triggered by pattern recognition receptors (PRRs) . There are two PRRs mainly response for bacterial infection: Toll-like receptors (TLRs) and Nod-like receptors (NLRs) [5, 6]. TLRs are located at the cell surface or within endosomal membranes. However NLRs mainly mediate cytosolic recognition of microbial molecules and promote their clearance . Our previous study have already proved that TLRs play a crucial role in regulation inflammation induced by S. aureus in bMECs . However the regulation effect of NLRs on S. aureus intracellular is still not clear, which challenge us for further detailed investigations and understanding.
Unlike TLR2, NLRs were capable to form inflammasomes in response to their specific stimulators [9, 10]. Among them the most characterized member of the NLR family is the NLRP3 inflammasome . Many studies have provided the activation process of NLRP3 pathway. Briefly, NlRP3 inflammasome composed of NLRP3, ASC and caspase-1, the activation of NLRP3 inflammasome ultimately process pro-IL-1β into IL-1β. Moreover, induce inflammatory response [12, 13]. Originally NLRP3 was hypothesized to be a cytosolic receptor. However with the deepening study, it seems highly improbable that NLRP3 acts as a receptor to directly bind to bacterial stimuli. ROS, produced by many known activators of NLRP3 inflammasomes, are shown to be a critical mechanism triggering NLRP3 inflammasome formation . Furthermore S. aureus have been found to activate the NLRP3 inflammasome in monocytes/macrophages leading to inflammation . However whether ROS offers a linked to the S. aureus infection and the antivation of NLRP3 inflammasome in bMECs is still unknown.
Se, an essential micronutrient, is a widely used feedstuff additive in dairy industry for a series of biology function such as antioxidant and immune anti-inflammation [16, 17]. Some research has indicated that Se deficiency is associated with an increased incidence of placental retentions, metritis, mastitis, susceptibility to infections and reduced fertility . On dairy industry, studies demonstrated adding Se in dietary could affect the innate and the adaptive immune responses to mastitis . The underlying mechanisms of Se in regulating mastitis is complicated. Our previous studies have confirmed that Se could ameliorates S. aureus-induced inflammation in bovine mammary epithelial cells by inhibiting activation of TLR2 signaling pathways. However further research is needed to determine whether NLRP3 pathway is involved in mastitis induced by S. aureus and whether Se is involved in the regulation of NLRP3 pathway in bMECs.