Broiler chickens are highly sensitive to high ambient temperatures due to their feathers, lack of skin sweat glands, and high productivity. Heat stress (HS) is a major concern for the poultry industry because it negatively affects growth as well as immune functions, which increase the potential risk of infectious disease outbreaks. Therefore, it is vital to elucidate HS's effect on the avian immune system, especially considering the global rise in average surface temperature. Our study identified a series of immunological disorders in heat-stressed broiler chickens. We exposed 22-day-old broiler chickens to a continuous HS condition (34.5 ± 0.5 • C) for 14 days and immunized them with a prototype bovine serum albumin (BSA) antigen. The plasma and lymphoid tissues (thymus, bursa of Fabricius, and spleen) were harvested at the end of the experiments to investigate the induction of BSA-specific immune responses. Our results revealed that plasma titers of immunoglobulin (Ig)Y, IgM, and IgA antibodies specific for BSA were lower than those of thermoneutral chickens immunized with BSA. Furthermore, the spleens of the heat-stressed broiler chickens displayed severe depression of Bu1 + B cells and CD3 + T cells, including CD4 + T cells and CD8 + T cells, and lacked a fully developed germinal center (GC), which is crucial for B cell proliferation. These immunological abnormalities might be associated with severe depression of CD4 − CD8 − or CD4 + CD8 + cells, which are precursors of either helper or killer T cells in the thymus and Bu1 + B cells in the bursa of Fabricius. Importantly, HS severely damaged the morphology of the thymic cortex and bursal follicles, where functional maturation of T and B cells occur. These results indicate that HS causes multiple immune abnormalities in broiler chickens by impairing the developmental process and functional maturation of T and B cells in both primary and secondary lymphoid tissues.

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It has been shown that oleuropein, a phenolic compound in the fruit and leaves of the olive tree (Olea europaea) induces mammalian uncoupling protein 1 (UCP1) expression via an increased secretion of noradrenaline and adrenaline. This study investigated the effects of oleuropein on avian UCP (avUCP) expression as well as genes related to mitochondrial oxidative phosphorylation and biogenesis in cultured avian muscle cells, together with reactive oxygen species generation. Oleuropein induced avUCP as well as peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor-1 (NRF1), mitochondrial transcription factor A (TFAM) and ATP5a1 (a component of mitochondrial adenosine triphosphate synthase) gene expression and cytochrome c oxidase activity, indicating the induction of mitochondrial biogenesis. Sirtuin-1 (SIRT1) gene expression was also up-regulated by this compound, which could contribute to an increase in PGC-1α activity. Oleuropein suppressed the level of superoxide generation per mitochondrion, possibly via the up-regulation of avUCP and manganese superoxide dismutase (MnSOD) expression. Based on these findings, this study is the first to show that oleuropein may induce avUCP expression in avian muscle cells independent of the catecholamines, in which PGC-1α may be involved.

Obesity is a major global lifestyle disorder associated with gut microbiota. The health benefits of eggshell membrane (ESM) have been shown in previous reports, particularly as regards gut microbiota composition. Here, we investigated whether ESM improves lipid metabolism and alters gut microbiota in high‐fat diet‐fed mice. A total of 20 C57BL/6J mice aged 6 weeks were given either a control diet (CON), high‐fat diet (HFD), or high‐fat diet + 8% ESM powder (HESM) for 20 weeks. ESM supplementation in HFD‐fed mice reduced plasma triglycerides (TG) and liver total cholesterol (TC) and upregulated the expression of lipid metabolism genes carnitine palmitoyltransferase 1A and suppressor of cytokine signaling 2. Microbiota analysis showed increased relative abundance of the anti‐obesity bacterium, Lactobacillus reuteri, at 4, 12, and 16 weeks and reduced the abundance of inflammation‐related Blautia hydrogenotrophica, Roseburia faecis, and Ruminococcus callidus at 12 and 20 weeks. ESM‐supplemented mice had increased cecal isobutyrate, negatively correlated with B. hydrogenotrophica and Parabacteroides goldsteinii abundance. The results indicate that ESM supplementation in HFD‐fed mice reduced plasma TG and liver TC, possibly through alteration of lipid metabolism gene expression and gut microbiota composition, suggesting that ESM may be effective in obesity management.

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Several genome-wide association studies (GWASs) have reported the association between genetic variants and the habitual consumption of foods and drinks; however, no association data are available regarding the consumption of black tea. The present study aimed to identify genetic variants associated with black tea consumption in 12,258 Japanese participants. Data on black tea consumption were collected by a self-administered questionnaire, and genotype data were obtained from a single nucleotide polymorphism array. In the discovery GWAS, two loci met suggestive significance (p < 1.0 × 10−6). Three genetic variants (rs2074356, rs144504271, and rs12231737) at 12q24 locus were also significantly associated with black tea consumption in the replication stage (p < 0.05) and during the meta-analysis (p < 5.0 × 10−8). The association of rs2074356 with black tea consumption was slightly attenuated by the additional adjustment for alcohol drinking frequency. In conclusion, genetic variants at the 12q24 locus were associated with black tea consumption in Japanese populations, and the association is at least partly mediated by alcohol drinking frequency.

Heat stress (HS) stimulates mitochondrial reactive oxygen species (ROS) production and protein degradation in skeletal muscle. The present study investigated the stimulatory effects of HS-induced mitochondrial ROS production on the ubiquitin-proteasome protein degradation system in primary cultured avian muscle cells. Cells were isolated from the breast muscle of neonatal chicks, and then grown for 48 h. Thereafter, the cells were subjected to 37℃ or 41℃ (HS). Exposure to 6 h of HS treatment significantly decreased the cellular protein content compared to that of normal cells, an effect was completely suppressed by the addition of a proteasome-specific inhibitor. Whereas the mRNA levels of the 20S proteasome C2 subunit, which is one of the subunits of the 26S proteasome, did not change at any time during HS treatment (1, 3, 6 h), the mRNA levels of atrogin-1 and muscle ring-finger protein 1, both of which are muscle-specific ubiquitin ligases, increased after 1 h of HS but then decreased to near-normal values with time. Intracellular ROS production (the sum of H 2 O 2 , hydroxyl radicals, peroxyl radicals, peroxynitrite) did not change in the 1 h HS-exposed cells, but was significantly increased after 3 h and 6 h of HS. Mitochondrial superoxide production was significantly increased after 1 h of HS, which might increase the mRNA expression of ubiquitin ligase in muscle cells. In cells pretreated with 4-hydroxy TEMPO, which is able to decrease mitochondrial superoxide production, the increases in mitochondrial superoxide production and ubiquitin ligase mRNA levels observed after 1 h of HS were suppressed. The protein content of these cells was not decreased, which was observed after the longest period of HS (6 h). These findings suggest that mitochondrial superoxide production may play an important role in activating the ubiquitin-proteasome system, probably via the induction of ubiquitin ligases, in HS-exposed muscle cells.

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