Goldsteinacevedo0604

In avian species, maternal immunoglobulin Y (IgY) is transferred from the blood to the yolks of maturing oocytes; however, the mechanism underlying this transfer is unknown. To gain insight into the mechanisms of maternal IgY transfer into egg yolks, IgY-depleted chickens were generated by removing the bursa of Fabricius (bursectomy) during egg incubation, and their egg production and IgY transport ability into egg yolks were determined. After hatching, blood IgY concentrations of the bursectomized chickens decreased gradually until sexual maturity, whereas those of IgA remained low from an early stage of growth (from at least 2 wk of age). NVS-STG2 in vivo Chickens identified as depleted in IgY through screening of blood IgY and IgA concentrations were raised to sexual maturity. At 20 wk of age, both blood and egg yolk IgY concentrations in the IgY-depleted group were 600-fold lower than those of the control group, whereas egg production did not differ between the groups. Intravenously injected, digoxigenin-labeled IgY uptake into the egg yolk was approximately 2-fold higher in the IgY-depleted chickens than in the controls, suggesting that IgY depletion may enhance IgY uptake in maturing oocytes. DNA microarray analysis of the germinal disc, including the oocyte nucleus, revealed that the expression levels of 73 genes were upregulated more than 1.5-fold in the IgY-depleted group, although we could not identify a convincing candidate gene for the IgY receptor. In conclusion, we successfully raised IgY-depleted chickens presenting a marked reduction in egg yolk IgY. The enhanced uptake of injected IgY into the egg yolks of the IgY-depleted chickens supports the existence of a selective IgY transport mechanism in maturing oocytes and ovarian follicles in avian species. The intestinal tract harbors a diverse community of microbes that have co-evolved with the host immune system. Although many of these microbes execute functions that are critical for host physiology, the host immune system must control the microbial community so that the dynamics of this interdependent relationship is maintained. To facilitate host homeostasis, the immune system ensures that the microbial load is tolerated, but anatomically contained, while remaining reactive to microbial invasion. Although the microbiota is required for intestinal immune development, immune responses regulate the structure and composition of the intestinal microbiota by evolving unique immune adaptations that manage this high-bacterial load. The immune mechanisms work together to ensure that commensal bacteria rarely breach the intestinal barrier and that any that do invade should be killed rapidly to prevent penetration to systemic sites. The communication between microbiota and the immune system is mediated by the interact receptor-expressing T cells are lymphocytes that are uniquely present in the mucosa. In addition, of the γδT cells in the intestinal lamina propria, there are significant numbers of IL-17-producing T cells and regulatory T cells. The accumulation and function of these mucosal leukocytes are regulated by the presence of intestinal microbiota, which regulate these immune cells and enhance the mucosal barrier function allowing the host to mount robust immune responses against invading pathogens, and simultaneously maintains immune homeostasis. This study was conducted to assess the growth performance and immunological effects of vaccination-induced stress on broilers. The chickens were administered 0, 2, 4, 8, and 16 doses of live LaSota Newcastle disease (ND) vaccine and slaughtered on the 1st, 7th, 14th, and 21st day post vaccination. The results showed that the serum antibody titers after Newcastle disease virus (NDV) vaccination were elevated at day 7 post vaccination, peaked at day 14, then declined by day 21. Interestingly, the antibody titers peaked at 2 doses, and no further dose-dependent titer increases were observed. This study demonstrated that vaccination-induced stress increased serum adrenocorticotropic hormone and cortisol, affected growth performance (average daily gain, average daily feed intake, and feed conversion ratio), and triggered apoptosis in spleen lymphocytes by downregulating the ratio of Bcl-2 to BAX and upregulating the gene expressions of caspase-3 and -9, which was concordant with the activation of the enzymatic activities of caspase-3 and -9. This study suggests that NDV vaccine doses in broilers must be controlled judiciously because increasing the number of doses resulted in increased lymphocyte apoptosis while the peak of the antibody titer and optimal growth performance were achieved at a low number of doses (2 doses). Infectious bronchitis (IB) causes severe economic losses to the poultry industry worldwide owing to frequent emergence of novel infectious bronchitis virus (IBV) variants, which potentially affect the effectiveness of the currently used IBV vaccine. Therefore, continuous monitoring of IBV genotypes and lineages recently circulating in chickens worldwide is essential. In this study, we characterized the complete S1 gene from 120 IBVs circulating in chickens in Thailand from 2014 to 2016. Phylogenetic analysis of the complete S1 gene of 120 Thai IBVs revealed that the 2014-2016 Thai IBVs were divided into 3 lineages (GI-1, GI-13, and GI-19) and a novel IBV variant. Our results also showed that GI-19 lineage has become the predominant lineage of IBV circulating in chicken flocks in Thailand from 2014 to 2016. It is interesting to note that a novel IBV variant, which was genetically different from the established IBV lineages, was identified in this study. The recombination analysis demonstrated that this novel IBV variant was a recombinant virus, which was originated from the GI-19 and GI-13 lineage viruses. In conclusion, our data demonstrate the circulation of different lineages of IBV and the presence of a novel recombinant IBV variant in chicken flocks in Thailand. This study highlights the high genetic diversity and continued evolution of IBVs in chickens in Thailand, and the importance of continued IBV surveillance for effective control and prevention of IB.