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

Background: Yak (Bos grunniens) mainly inhabiting Tibet Plateau, displayed a high incidence of diarrhea due to harsh living environment and nutritional deficit. Gut microbial community has been reported to be closely related to many diseases including diabetes, obesity and inflammatory bowel disease, but information regarding diarrheic influence on gut microbiota in yaks remains scarce. Here, this study was performed to investigate the gut bacterial and fungal alternations of diarrheic yaks. Results: Results revealed that the gut bacterial and fungal communities of diarrheic yaks showed a distinct decline in alpha diversity, accompanied by significant shifts in taxonomic compositions. Specifically, diarrhea caused a distinct increase in the relative abundance of 1 phylum and 8 genera as well as a distinct decrease in 3 phyla and 30 genera. Fungal taxonomic analysis indicated that the relative richness of 1 phylum and 2 genera dramatically increased, whereas the relative richness of 2 phylum and 43 genera significantly decreased during diarrhea. Surprisingly, 2 bacterial genera and 5 fungal genera even cannot be detected in the gut microbiota of diarrheic yaks. Conclusions: In summary, this study indicated that the gut bacterial and fungal compositions and diversities of yaks altered significantly during diarrhea. Moreover, these findings also contribute to understanding the gut microbial composition and diversity of yaks and developing strategies to alleviate and prevent diarrhea from gut microbial perspective. [ABSTRACT FROM AUTHOR]

This study was conducted to examine the effect of active dry yeast (ADY) supplementation on lactation performance, ruminal fermentation patterns, and CH 4 emissions and to determine an optimal ADY dose. Sixty Holstein dairy cows in early lactation (52 ± 1.2 DIM) were used in a randomized complete design. Cows were blocked by parity (2.1 ± 0.2), milk production (35 ± 4.6 kg/d), and body weight (642 ± 53 kg) and assigned to 1 of 4 treatments. Cows were fed ADY at doses of 0, 10, 20, or 30 g/d per head for 91 d, with 84 d for adaptation and 7 d for sampling. Although dry matter intake was not affected by ADY supplementation, the yield of actual milk, 4% fat-corrected milk, milk fat yield, and feed efficiency increased quadratically with increasing ADY supplementation. Yields of milk protein and lactose increased linearly with increasing ADY doses, whereas milk urea nitrogen concentration and somatic cell count decreased quadratically. Ruminal pH and ammonia concentration were not affected by ADY supplementation, whereas ruminal concentration of total volatile fatty acid increased quadratically. Digestibility of dry matter, organic matter, neutral detergent fiber, acid detergent fiber, nonfiber carbohydrate, and crude protein increased quadratically with increasing ADY supplementation. Supplementation of ADY did not affect blood concentration of total protein, triglyceride, aspartate aminotransferase, and alanine aminotransferase, whereas blood urea nitrogen, cholesterol, and nonesterified fatty acid concentrations decreased quadratically with increasing ADY supplementation. Methane production was not affected by ADY supplementation when expressed as grams per day or per kilogram of actual milk yield, dry matter intake, digested organic matter, and digested nonfiber carbohydrate, whereas a trend of linear and quadratic decrease of CH 4 production was observed when expressed as grams per kilogram of fat-corrected milk and digested neutral detergent fiber. In conclusion, feeding ADY to early-lactating cows improved lactation performance by increasing nutrient digestibility. The optimal ADY dose should be 20 g/d per head. [ABSTRACT FROM AUTHOR]