Journal of Animal Science and Biotechnology最新文献

Background: Heat stress (HS) can impair boar testicular function, leading to reproductive issues. However, chlorogenic acid (CGA) has been shown to mitigate HS-induced damage in various livestock and poultry species. Prepuberty is an important stage of testicular development in boars after birth. However, the protective effect of CGA on testicular HS injury during prepuberty boars and the underlying mechanisms are still not fully understood.

Results: In vivo, a total of 30 healthy boars with similar body weights and ages were obtained and randomly divided into 3 groups, which were fed a basal diet supplemented with CGA 0 (the ND_TN group), 0 (the ND_HS group) or 1,000 (the CGA_HS group) mg/kg. After being fed for 28 d, all the groups, except the ND_TN group, were treated with high temperature for 7 d, after which samples were collected from the boars and analysed. The results showed that CGA significantly mitigated the HS-induced reduction in T-AOC content in testicular tissue and sperm density. Mechanistically, multiomics analysis revealed that the genes differentially expressed by CGA and HS were predominantly associated with the glutathione metabolism pathway. The combined analysis of transcriptomics and proteomics revealed that only BLVRA was affected by both HS and CGA when the mRNA and protein levels of a gene showed differential expression with the same trend. In vitro studies confirmed that CGA modulated GPX3 expression via BLVRA, affected GPx activity, and attenuated HS-induced ROS accumulation.

Conclusions: In conclusion, prepubertal HS impairs the spermatogenic capacity of boars. BLVRA may mediate the testicular protective effect of CGA, although in vivo validation of this pathway is needed. This study contributes to elucidating the mechanisms underlying the effects of HS on prepubertal boar testicular development using multiomics approaches, laying a foundation for the potential utilization of CGA in swine production.

Background: Sphingolipids (SL) are key regulators of inflammatory processes, yet their roles in dairy cows remain poorly understood. This study investigated the effects of inflammation (plasma haptoglobin concentration), ketosis, and mastitis on plasma SL profiles in Holstein cows sampled seven days postpartum. From a cohort of 427 cows across 25 farms, 80 animals were classified into four groups: inflammation (n = 20), ketosis (n = 19), mastitis (n = 21), and healthy controls (n = 20). Plasma SL were quantified by targeted HPLC-MS/MS, while cytokines were quantified with a 15-plex bead-based assay. Both univariate and multivariate analyses were applied to assess pathological effects, along with SL ratios and correlations between SL and cytokines.

Results: Systemic inflammation detected through the haptoglobin measure induced the most pronounced alterations in SL metabolism, characterized by elevated dihydrosphingomyelins (DHSM) and lactosylceramides (LacCer), higher C22-24:C16 ratios, and lower unsaturated:saturated ratios in ceramides (Cer) and sphingomyelins (SM). Although total Cer, SM, and the Cer:SM ratio remained unchanged, specific reductions were observed in both Cer and SM in C14, Cer C18:1, SM C16:1, and SM C23:1, whereas SM C25:0 and C26:0 increased. Sphingosine-1-phosphate (So1P) was positively correlated with IL-10 as well as IL-1α and TNFα, while C18-20 Cer correlated positively with multiple pro-inflammatory cytokines and chemokines such as CXCL8 and CCL2. Ketosis induced subtler changes, primarily an increase in plasma DHSM and DHSM:SM ratio (driven by C16:0), an increase in C22-24:C16 DHCer ratio, and a decrease in both LacSo:LacCer and unsaturated:saturated ratios in C23-SM. In this group, So1P correlated positively with CXCL8 and CCL2. Moreover C18-20 Cer and DHCer were positively associated with CXCL8, CCL2, CCL3, and CCL4, which also showed correlations with most LacCer species. Analysis of chronic mastitis cases yielded a clear separation from controls in multivariate analysis but only minimal changes in SL concentrations and ratios, maybe due to the localized nature of the inflammatory response.

Conclusions: In summary, heightened inflammatory response in early post-partum is associated with the strongest systemic effects on SL metabolism, followed by ketosis, while mastitis induced only modest alterations. These findings highlight condition-specific patterns of SL regulation postpartum and suggest potential immunometabolic biomarkers of disease.

Background: Selective breeding for disease resistance is an effective strategy to control duck hepatitis A virus type 3 (DHAV-3) in waterfowl. However, the mechanism underlying resistance remains poorly understood, particularly those associated with antioxidant defense, intestinal development and host-microbiota interactions.

Method: A total of 100 1-day-old Pekin ducklings were used in this study with 50 DHAV-3 susceptible and resistant ducks, respectively. Samples were collected at 7 days post-hatching (D7), D21 and D42, 10 birds per group. We compared DHAV-3 resistant and susceptible ducks during early development with respect to immune organ indices, antioxidant capacity, intestinal morphology, barrier-related gene expression and cecal microbiota.

Result: Resistant ducks exhibited higher spleen indices and stronger antioxidant capacity, characterized by increased superoxide dismutase, reduced glutathione, and total antioxidant capacity, along with lower malondialdehyde levels at D7 and D21. In contrast, susceptible ducks showed compensatory thymus hypertrophy and delayed development of antioxidant defense and intestinal maturation. Ileal morphology revealed greater villus height and width with more regular arrangement in resistant ducks at D7, whereas these differences diminished at D21 and D42. Gene expression analysis demonstrated higher early expression of the tight junction proteins CLDN1 and CLDN3 in resistant ducks, while susceptible ducks displayed elevated MUC2 and OCLN, suggesting stress induced compensatory responses. Cecal microbiota analysis revealed distinct colonization patterns in early development. Resistant ducks were enriched with Firmicutes and beneficial genera such as Enterococcus and Lactobacillus, whereas susceptible ducks harbored higher abundances of Bacteroidota and potentially opportunistic taxa. Microbial diversity increased with age in both groups, but resistant ducks displayed more orderly succession and enrichment of SCFA producing genera, including Subdoligranulum and Phascolarctobacterium, which positively correlated with plasma antioxidant indices.

Conclusion: DHAV-3 resistant ducks exhibit early advantages in antioxidant defense, intestinal barrier development and colonization by beneficial microbiota, which collectively contribute to enhanced disease resistance. These findings highlight the synergistic roles of host physiology and gut microbiota in shaping resistance. In the future, integrating genomic selection with microbiota modulation and antioxidant interventions may accelerate the breeding of highly resistant duck lines and provide scientific evidence and practical strategies for controlling duck viral hepatitis.

Background: Endometrial receptivity (ERE) is a transient uterine state that determines the success of blastocyst implantation; however, the epigenomic regulation underlying ERE establishment in goats remains unclear. Here, we profiled transcriptional and epigenomic features of endometrial tissues from pregnant goats during the peri-implantation window and nonpregnant control goats in the regressed luteal phase to uncover the transcriptional regulatory networks responsible for ERE establishment in goats, utilizing RNA-seq, ATAC-seq, and H3K27ac CUT&Tag.

Results: A total of 3,143 differentially expressed genes (DEGs) were identified, accompanied by significant alterations in chromatin accessibility and H3K27ac modifications between receptive and non-receptive endometria. The targeted genes associated with these epigenetic changes were significantly enriched in pathways related to cell adhesion, immune tolerance, and embryo attachment. Motif enrichment and transcription factor (TF) footprinting analyses identified members of the FOS/JUN, SOX, HNF1, CEBP, and BATF families as candidate regulators, implicating downstream genes involved in ERE establishment, including SPP1, FOXO1, KLF4/6, STAT1, IFI6, ITGB8, PLAC8, DUSP4, NR1D1, ISG15, RUFY4, and PIK3R3. In addition, numerous super-enhancers were identified, indicating regions of high regulatory activity and potential long-range gene-enhancers interactions in the endometrium. Integration of multi-omics datasets revealed a strong correlation (r > 0.7) among chromatin accessibility, H3K27ac activation, and the expression of 172 DEGs. Furthermore, a set of hub genes (KLF6, IFI6, MCL1, SDC4, SUSD6, MAFF, and IL6R) that appear to coordinate TF binding and distal super-enhancers activity associated with ERE establishment.

Conclusions: Our data provided an integrated epigenomic atlas of endometrial receptivity establishment in goats and identify candidate regulatory elements and transcription factors that may orchestrate uterine preparation for implantation. These findings offer valuable insights and testable targets for improving fertility in ruminant livestock.

Background: Undernutrition disrupts pregnant ewe's metabolic homeostasis and severely inhibits fetal growth and development. In this study, undernourished and nutrition-recovery pregnant sheep models and rumen epithelial cells were utilized to investigate the mechanisms behind undernutrition-induced disruptions in male fetal rumen metabolism and development.

Results: Maternal undernutrition significantly reduced male fetal rumen weight and papilla length, width and surface area. Maternal undernutrition extremely suppressed nutrient metabolism and energy production in male fetal rumen via JAK3/STAT3 signaling to inhibit cell cycle progression and male fetal rumen development, while maternal nutritional recovery partially restored metabolic inhibition but failed to alleviate male fetal rumen development. Meanwhile, 64 differentially expressed miRNAs (DEMs) were identified in male fetal rumen between undernourished ewes and controls. Novel miR-736 was overexpressed both in male fetal rumen of undernourished and nutrition-recovery models. E2F transcription factor 2 (E2F2) and MYB proto-oncogene like 2 (MYBL2) were the intersection of male fetal rumen differentially expressed genes (DEGs) and DEMs target genes integrated analysis and were predicted as novel miR-736 target genes. Further, we confirmed that novel miR-736 targeted and downregulated E2F2 and MYBL2 expression levels. Silencing E2F2 and MYBL2 promoted apoptosis and inhibited S-phase entry in rumen epithelial cells.

Conclusions: In summary, maternal undernutrition disrupted male fetal rumen metabolism and elevated novel miR-736, which targeted and downregulated E2F2 and MYBL2 to inhibit cell cycle progression and promote apoptosis, finally inhibited male fetal rumen development. This study provides new insights into the epigenetic mechanisms underlying maternal undernutrition-induced male fetal rumen developmental deficits.

Background: Perilla frutescens seeds (PFS) are gaining recognition as a natural alternative to antibiotics in livestock, supporting sustainable farming and animal health. However, the underlying molecular mechanisms through which PFS influence host immune function and antioxidant capacity, especially via the gut-liver-muscle axis, remain largely unknown. This study employed an integrative multi-omics approach to elucidate how PFS supplementation modulates the microbiota-gut-liver-muscle axis and enhances immune and antioxidant functions in lambs.

Results: PFS supplementation markedly improved immune and antioxidant profiles, demonstrated by elevated serum levels of IL-10, IgM, IgG, GSH-PX, and SOD, and reductions in IL-1β, TNF-α, and MDA. Microbial analysis revealed elevated abundances of ruminal and intestinal taxa commonly associated with gut homeostasis and metabolic health (Christensenellaceae_R-7_group) and reduced levels of species with pathogenic or pro-inflammatory potential (Bacillus cereus and Clostridioides) in the ileum. Transcriptomic and metabolomic profiling of liver tissue indicated modulation of key inflammatory and bile acid signaling pathways, including the downregulation of TLR4, NLRP3, ATF3, CYP2J2, and LXR-α. PFS also increased hepatic concentrations of anti-inflammatory metabolites such as chlorquinaldol and indole-3-carboxaldehyde, while reducing levels of LysoPC(20:4) and phosphatidic acid. Correlation and mediation analyses revealed strong interconnections among gut microbiota, hepatic gene expression, lipid metabolites in liver and muscle, and systemic immune-antioxidant markers.

Conclusion: These findings highlight the microbiota-gut-liver-muscle axis as a central mechanism through which PFS enhances immune function and antioxidant capacity in lambs. PFS supplementation represents a promising nutritional strategy to improve healthy lamb production, supporting the development of antibiotic-free and sustainable livestock systems.

Background: An imbalance in the rumen microbiota caused by high-concentrate diets (HCD) is a significant endogenous trigger of mastitis. However, the underlying mechanisms remain largely unknown. Microbial extracellular vesicles (mEVs) are critical mediators of microbe-host communication. However, the role of mEVs in rumen microbiota-mediated mastitis has not yet been reported. In this study, we used an HCD-induced rumen microbiota dysbiosis model to investigate the role of mEVs-derived from rumen microbiota in the pathogenesis of mastitis.

Results: Our results indicate that HCD leads to mastitis and systemic inflammation. Meanwhile, HCD-fed goats exhibited substantial rumen microbiota dysbiosis and the disruption of the rumen barrier. Transplanting rumen microbiota from HCD goats into mice induced both mastitis and systemic inflammation in the recipients. Specifically, HCD increases the production of mEVs carrying microbial DNA, which can translocate across the compromised rumen barrier to the mammary gland, triggering a mammary inflammatory response via activation of the cGAS-STING-NF-κB/NLRP3 pathway. Furthermore, treating mice with mEVs isolated from the rumen fluid of HCD goats directly induced mastitis, whereas depletion of microbial DNA attenuated mEVs-induced mastitis.

Conclusion: Our findings suggest that HCD induces rumen microbiota dysbiosis and impairs rumen barrier function. This dysfunction leads to an increase in microbial DNA-containing mEVs, which subsequently leak into the mammary gland. Once there, these mEVs activate the cGAS-STING-NF-κB/NLRP3 signaling pathway, ultimately inducing mastitis. This study provides a new perspective on the "rumen microbiota-mammary gland axis" and enhances the understanding of the pathogenesis of mastitis.

Background: Selenium (Se) is an essential soil mineral that can be incorporated into animal feedstuffs. Because of a lack of soil Se in some regions, organic or inorganic supplementation strategies must be implemented to prevent deficiencies and promote optimal ovine health. Therefore, the objectives of this study were to assess how inorganic versus organic Se supplementation influenced ewe Se status and immune function during late gestation and postpartum. Dorset Rideau ewes (n = 110) were fed a Se deficient diet from gestation d 110 through postpartum d 49 and received one of four daily oral Se treatments diluted in 5 mL of sugar water: 0 mg Se, 0.3 mg inorganic Se, 0.3 mg organic Se, and 0.6 mg organic Se. Throughout the trial, the ewes received various immune challenges, including intramuscular immunizations with a novel antigen (ovalbumin; OVA) on trial d 0 and 10, an intradermal OVA challenge on d 20, and a lipopolysaccharide (LPS) endotoxin challenge on trial d 49.

Results: The organic Se treatment groups had higher serum Se concentrations on most trial days compared to the 0.3 mg inorganic and control groups (P < 0.05). No significant treatment differences were found for the dermal hypersensitivity response to OVA, anti-OVA antibody response, glutathione peroxidase activity, cytokine response, cortisol response, or rectal temperature (P > 0.05). However, 4 h post-LPS injection, the serum albumin concentration was significantly lower in the 0.3 mg inorganic group compared to both organic Se groups, potentially indicating a higher degree of inflammation in the ewes supplemented with the inorganic Se.

Conclusions: The results of this study indicate that organic Se supplementation can promote a higher Se status in ewes over time, but Se supplementation during this study period did not affect tested immunological parameters. This lack of difference in immune responsiveness between groups may be due to an absence of true serum Se deficiencies in the Se-deficient group or the levels of Se supplementation being insufficient to significantly improve immunocompetence.

There is increasing interest in developing reduced-crude protein (CP) diets for broiler chickens because their commercial adoption would generate a diverse range of advantages that would enhance the sustainability of the chicken-meat industry. However, the development of reduced-CP broiler diets is proving to be not straightforward, particularly when dietary CP reductions exceed 30 g/kg. The capacity of broilers to accommodate dietary CP reductions when offered maize-based diets is superior to their counterparts offered wheat-based diets. Numerous factors could be contributing to this difference but have yet to be identified with certainty. Maize-based, reduced-CP diets characteristically support better weight gains and efficiencies of feed conversion than wheat-based diets, but this better growth performance is associated with increased fat deposition, monitored as heavier relative abdominal fat-pad weights. This is an intriguing dichotomy. Insulin is a powerful anabolic hormone in mammalian species capable of promoting fat deposition, protein accretion and growth, but the importance of insulin in avian species is usually dismissed. This is because broiler chickens are considered both hyperglycaemic and resistant to insulin. However, the likelihood is that young broiler chickens are more sensitive to insulin than is generally recognised and the anabolic properties of insulin may be contributing to the diverse responses observed between maize and wheat in the context of reduced-CP diets. Dietary CP reductions may trigger increased plasma ammonia concentrations and metabolic acidosis, but both factors can influence insulin secretion and insulin resistance. Maize has slower rates of starch digestion and glucose absorption than wheat and it has been suggested that this generates a more sustained insulin release resulting in increased weight gains and fat deposition. If so, this could be driving the differences generated by the feed grain selected as the basis of reduced-CP diets. The intention of this review is to explore this proposition because if the causal factors of the differences between maize and wheat can be identified the development and acceptance of reduced-CP broiler diets should be accelerated.

Backgrounds: Deoxynivalenol (DON) is an abundant environmental pollutant in feed, posing serious health hazards to animals. However, whether DON triggers an imbalance in mitochondrial fission/fusion and the underlying mechanisms involved remain poorly understood. Our aim was to clarify whether mitochondrial fission or fusion proteins participated in DON-caused intestinal damage in pigs.

Methods: Firstly, two groups of weaning pigs were fed a basal diet, or basal diet supplemented with 4 mg DON/kg for 3 weeks. Additionally, another two groups of weaning pigs were given an oral gavage with 2 mg/kg body weight DON or an equivalent amount of normal saline. In addition, the involvement of mitochondrial fission or fusion proteins in DON-induced intestinal damage was further verified in intestinal porcine epithelial cell line (IPEC-1) by overexpressed plasmids of dynamin related protein 1 (Drp1) and mitofusin 2 (Mfn2) which were determined by animal studies. Finally, a mitochondrial fusion promotor M1 was used in IPEC-1 cells to explore the role of Mfn2 in DON-induced intestinal damage.

Results: Dietary DON caused jejunal damage and inflammation, reduced intestinal Drp1, mitofusin 1 (Mfn1) and Mfn2, and induced cell apoptosis. DON gavage also impaired jejunal structure and led to decreased Drp1 and Mfn2, and increased cell apoptosis. Moreover, DON challenge also resulted in cell damage and mitochondrial dysfunction, accompanied by abnormal protein expression of mitochondrial fission/fusion proteins and increased cell apoptosis in IPEC-1 cells. Subsequently, Mfn2, but not Drp1 overexpression plasmid restored mitochondrial fission/fusion protein expression, suppressed cell apoptosis, mitigated cell damage and mitochondrial dysfunction in IPEC-1 cells after DON challenge. Finally, M1 alleviated DON-induced reduction of Mfn2 protein and cell apoptosis, rescued mitochondrial dysfunction, barrier function impairment and cell damage.

Conclusions: Overall, our study demonstrates that DON exposure triggers Mfn2 protein dysregulation, which in turn mediates DON-induced intestinal epithelial damage in piglets.