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1.
Vet Res Commun ; 43(2): 131-142, 2019 May.
Article in English | MEDLINE | ID: mdl-31055768

ABSTRACT

In this study, we investigated the effects of probiotic, acidifier and synbiotic supplementation on growth performance, mortality rate, intestinal gene expressions, fecal shedding, and organs colonization induced by Escherichia coli in broiler chickens. Six experimental groups were included; negative control group (NC), positive control group (PC), probiotic group (PR), acidifier group (AC), synbiotic group (SY) and colistin sulfate group (CS). Chickens in groups NC and PC were fed a basal diet, while chickens in groups PR, AC, SY, and CS were fed a basal diet containing probiotic, acidifier, synbiotic and colistin sulfate, respectively from the 1st day to the 28th day of age. At 7 days of age, all groups (not NC) were orally challenged with 0.5 ml (1.0 × 109 CFU/ml) E. coli O78. The dietary supplementation of acidifier and synbiotic were sufficient to quell the devastating effects of E. coli infection in broilers. Growth performances represented by body weight gain, feed intake and feed conversion ratio were significantly improved as well as, mortalities were prevented whilst the ileal pro-inflammatory gene expressions (IL-6, IL-8, IL-13, TLR-4, IFN-γ, LITAF, AvBD-2, and AvBD-9) were significantly downregulated and the anti-inflammatory cytokine (IL-10) was significantly increased. In addition, E. coli fecal shedding and organs colonization was significantly diminished. It was concluded that the addition of both acidifier and synbiotic to the diet of broilers infected with E. coli could modulate the intestinal inflammatory responses induced by E. coli infection and minimized the inflammation-induced damage which resulted in improvement in growth performance, prevention of mortalities and reduction of E. coli environmental contamination.


Subject(s)
Dietary Supplements , Escherichia coli Infections/veterinary , Gene Expression Regulation/drug effects , Poultry Diseases/physiopathology , Probiotics/pharmacology , Animals , Chickens , Colistin/pharmacology , Eating/drug effects , Escherichia coli , Escherichia coli Infections/physiopathology , Intestines/drug effects , Synbiotics , Weight Gain/drug effects
2.
Reprod Domest Anim ; 53(2): 352-358, 2018 Apr.
Article in English | MEDLINE | ID: mdl-29164710

ABSTRACT

The transition period is a critical time for dairy cows as the animal is subjected to the physiological stress accompanying parturition. Immunosuppression and health status were examined during this period in 80 Holstein cows. Blood samples were taken from each cow 3, 2 and 1 week before and after calving, and at calving (0 day). RNA was extracted and subjected to real-time PCR to determine mRNA levels for the immune-related genes TLR 2, 4, 6, 7 and ß-defensin 5 in addition to the reproduction-related genes prolactin and IGF-I. Results showed significant up-regulation of pro-inflammatory-selected genes, TLR 4, 6 7 and ß-defensin 5 at the third-week post-calving; however, earlier periods had lower expression of such genes. In contrast, the immunosuppression biomarker TLR2 gene was up-regulated at calving and 1 week after parturition and then down-regulated again at second and third week. Prolactin and IGF-I genes expression levels were significantly and gradually increased mainly post-partum. This research highlights that the expression patterns of TLRs, BNBD5, PRL and IGF-I could be biomarkers to follow up immune and reproductive status of dairy cow at peri-parturient period to predict the most susceptible risk time for disease incidence and to build up management protocol.


Subject(s)
Cattle/physiology , Peripartum Period/physiology , Transcriptome/physiology , Animals , Biomarkers , Cattle/immunology , Cattle/metabolism , Female , Immunosuppression Therapy/veterinary , Insulin-Like Growth Factor I/genetics , Insulin-Like Growth Factor I/metabolism , Peripartum Period/immunology , Peripartum Period/metabolism , Prolactin/genetics , Prolactin/metabolism , RNA, Messenger , Stress, Physiological/physiology , Toll-Like Receptors/genetics , Toll-Like Receptors/metabolism , beta-Defensins/genetics , beta-Defensins/metabolism
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