Introduction: Salmonella enterica serovars Enteritidis and Typhimurium represent the major serovars associated with human salmonellosis. Contamination of meat products with these serovars is considered the main source of infection. Methodology: In this study, 100 raw chicken meat samples were investigated for the presence of Salmonella spp., which were subsequently identified based on biochemical and serological tests as well as matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) profile. Furthermore, the isolated serovars were examined using multiplex polymerase chain reaction (PCR) for the presence of virulence genes suspected to have a role in infection. Results: S. Enteritidis was isolated from two samples (2%), while S. Typhimurium was isolated from three samples (3%) of chicken meat. Of the 17 examined virulence genes using multiplex PCR, the sitC, sopB, sifA, lpfC, spaN, sipB, invA, spiA, and msgA genes were detected in S. Enteritidis. However, the sitC, iroN, sopB, sifA, lpfC, spaN, sipB, invA, and tolC genes were successfully amplified in S. Typhimurium. Conclusions: The detection of S. Enteritidis and S. Typhimurium in meat, even at low incidence, has important implications. In addition, the data presented here is the first attempt to identify a wide range of virulence genes in Egyptian Salmonella isolates recovered from meat products. A strict public health and food safety regime is urgently needed in order to decrease the human health hazard risk associated with salmonellosis.
The current study conducted to investigate the effects of a multi-strain commercial probiotic mix and prebiotic (isomaltooligosaccharide, IMO) on broiler performance parameters, cecal microbiota composition, and protection against challenge with avian pathogenic Escherichia coli (APEC) O78. For this purpose, 101-day-old Cobb chicks were randomly allocated into four experimental groups (G)-G01: basal diet, G02: basal diet and challenged with E. coli O78 at 28 days old, G03: basal diet with probiotic mix and challenged with E. coli O78 at 28 days old, and G04: basal diet with IMO and challenged with E. coli O78 at 28 days old. Results showed that weekly body weights in G03 were heavier (P < 0.05) than those of G01 and G02 at the fourth and fifth week. The body gain at the fourth and fifth week was higher (P < 0.05) in G03 than those of the other groups. The hot carcass weight (g) was significantly higher in broiler chickens kept in G03 and G04 compared with those in the control groups (G01 and G02). The probiotic mix and IMO significantly increased the total lactobacilli and total lactobacilli-enterococci populations in the ceca of treated broilers, respectively compared with those in the control groups. The treated broilers (G03 and G04) also showed lower mortality percentage and E. coli recovery rates the liver and spleen than those in G02. It was concluded that probiotic mix or IMO significantly improved the growth performance and modulated the intestinal microbiota of broiler chickens challenged with APEC O78.
In this study, the effect of lipopolysaccharide (LPS) on protein synthesis (PS) and intracellular signaling factors that regulate it have been investigated in C2C12 murine-derived myotubes. In particular, the role of Akt/mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinases (MAPKs) [p38 and extracelluar regulated protein kinase (ERK1/2)] have been examined. The direct effect of LPS on PS was measured at 3 and 18 h. LPS significantly decreased PS at 3 h but not at the 18-h time point. This effect was preceded by decreased Akt phosphorylation at 5 and 30 min after LPS administration. The mTOR phosphorylation exhibited a long time dose-dependent increase at all the time points. Similarly, the activity-related phosphorylation of p38 and ERK1/2 significantly increased in a time- and dose-dependent manner at all the time points. Polymyxin B abolished the LPS-induced decrease in PS rate. The phosphatidylinositol 3-kinase inhibitor LY-0294002 in combination with LPS significantly decreased the rate of PS by 81% and alone by 66%, respectively, for the 3- and 18-h time points, whereas p38 and ERK inhibitors in combination with LPS significantly decreased the rate PS rate at the 18-h time point by 41% and 59%, respectively, compared with control cells. In conclusion, LPS alone transiently decreased the rate of PS by 50% at 3 h; this effect is most likely mediated via the Toll-like receptor 4 (TLR4)-Akt/mTOR pathway, and both p38 and ERK when inhibited in the presence of LPS at 3 h have a similar effect in preventing the LPS-induced reduction in PS.
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