Journal of Animal Science and Biotechnology最新文献

Background: Mastitis is known to alter milk lipid yield, but its effects on lipid composition in blood and milk remain less understood. This study investigated changes in fatty acid (FA) composition in blood lipid fractions and milk of dairy cows following an intramammary lipopolysaccharide (LPS) challenge and explored potential links associated with these changes. We hypothesized that intramammary LPS infusion would alter the FA composition of blood lipid fractions, and that milk FA composition would reflect these changes. Furthermore, we hypothesized that prostaglandin E₂ (PGE₂) would be associated with changes in both blood and milk FA composition, functioning as a potential mediator of these changes.

Results: Ten lactating cows were split into two groups. The treatment group received intramammary infusions of 50 μg Escherichia coli LPS in both quarters of one udder half to induce clinical mastitis, and saline infusions in the quarters of the opposite udder half; the control group received saline infusions in one udder half only. Blood and foremilk were collected from individual cows or glands at -1, 3, 6, 12, and 24 h post-infusion. Blood lipids were fractionated into cholesterol esters, free fatty acids (FFA), phospholipids (PL), and triacylglycerides (TAG). The FA composition was analyzed via gas-liquid chromatography. Total plasma TAG, FFA, and PGE₂ concentrations were measured by colorimetric assay or ELISA. Statistical significance was determined using mixed models with Tukey's test. Lipopolysaccharide infusion did not affect total plasma TAG and FFA concentrations but increased plasma PGE₂ concentrations and Δ9 desaturation indices in plasma TAG. A distinct shift in FA composition in plasma phospholipids and TAG was observed between the treatment and control groups at 6 and 12 h post-infusion. Specifically, LPS increased the proportion of n-6 polyunsaturated FA (18:2, 18:3, 20:3, 20:4, 20:5) and FA with less than 16 carbons while decreasing the saturated FA (18:0 and 20:0) in plasma TAG at 6 and 12 h. However, the milk FA composition remained unchanged.

Conclusion: Our findings indicate that transient intramammary LPS challenge influences systemic lipid metabolism without altering the milk FA composition, suggesting that mammary inflammatory responses affect blood lipids independently of milk lipid secretion.

Background: Follicular atresia, a complex degenerative process regulated by multiple molecular mechanisms, significantly affects female reproductive performance in animals. While granulosa cell (GC) apoptosis has been well established as a primary mechanism underlying follicular atresia, the potential involvement of ferroptosis, which is an iron-dependent form of regulated cell death, remains largely unexplored in chickens.

Results: Using a tamoxifen (TMX)-induced avian model of follicular atresia, we demonstrated that ferroptosis plays a critical role in follicular degeneration. Inhibition of ferroptosis through pharmacological agents significantly restored follicular function, underscoring its potential as a therapeutic target. Notably, we observed a significant upregulation of ubiquitin-specific peptidase 9, X-linked (USP9X) in GCs during atresia. Through comprehensive in vitro and in vivo investigations, we confirmed that USP9X facilitates follicular atresia by promoting ferroptosis in GCs. Mechanistically, USP9X induces ferroptosis by stabilizing Beclin1 through deubiquitination, thereby activating autophagy-dependent ferroptosis. This pathway was effectively suppressed by autophagy inhibitors, emphasizing the essential role of autophagy in USP9X-mediated ferroptosis.

Conclusions: Our findings provide the evidence that the USP9X-Beclin1 axis regulates autophagy-dependent ferroptosis during avian follicular atresia. These insights reveal novel molecular targets and potential genetic markers for improving reproductive efficiency in chicken breeding programs.

Background: To more effectively address the scarcity resources and elevated costs associated with fishmeal (FM), the utilization of cottonseed protein concentrate (CPC) as an alternative in aquaculture feeds has become increasingly prevalent. However, high levels of CPC substitution for FM have been reported to suppress the growth of fish and impair intestinal health. Hydrolysable tannin (HT) has been reported to exhibit biological activities such as anti-inflammatory and antioxidant activities, but whether the HT can generate positive biological effects on the intestinal health of largemouth bass (Micropterus salmoides) remains unknown. Largemouth bass (initial weight: 6.03 ± 0.01 g) were subjected to an 8-week feeding trial with three different diets: a basic diet (named as the NC), a high CPC diet (in which CPC replaced 75% of the FM protein in the NC diet, named as the HC), and an additive diet (1.25 g/kg of the HT was added to the HC diet, named as the HCH) to explore the potential benefits of HT on intestinal health.

Results: The HC treatment significantly reduced the weight gain rate of fish, increased the feed conversion ratio, and induced intestinal inflammation. However, the HCH treatment could alleviate the adverse impacts of the HC diet, as evidenced by the promotion of growth and feed utilization, increased activity of digestive enzymes and antioxidant capacities, downregulated expression of pro-inflammatory factors, and maintenance of the integrity of intestinal barrier. Metabolomic analysis revealed that HCH treatment could reduce the pro-inflammatory active substances produced by arachidonic acid metabolism, including prostaglandin F_2α (PGF_2α) and leukotriene B₄ (LTB₄). Transcriptomic results indicated that dietary HT might alleviate intestinal inflammation by suppressing the activation of the NF-κB signaling pathway. Furthermore, correlation analysis demonstrated that the metabolites PGF_2α and LTB₄, derived from arachidonic acid, exhibited a significant positive correlation with the expression of genes associated with pro-inflammatory responses within the NF-κB signaling pathway.

Conclusions: The study indicates that the HT mitigates the growth retardation and intestinal inflammation resulting from the HC diet on largemouth bass.

Background: Backfat thickness (BFT) is a vital economic trait in pigs, reflecting subcutaneous fat levels that affect meat quality and production efficiency. As a complex trait shaped by multiple genetic factors, BFT has been studied using genome-wide association studies (GWAS) and linkage analyses to locate fat-related quantitative trait loci (QTLs), but pinpointing causal variants and genes is hindered by linkage disequilibrium and limited regulatory data. This study aimed to dissect the QTLs affecting BFT on Sus scrofa chromosome 1 (SSC1), elucidating regulatory variants, effector genes, and the cell types involved.

Results: Using whole-genome genotyping data from 3,578 pigs and phenotypic data for five BFT traits, we identified a 630.6 kb QTL on SSC1 significantly associated with these traits via GWAS and fine-mapping, pinpointing 34 candidate causal variants. Using deep convolutional neural networks to predict regulatory activity from sequence data integrated with detailed pig epigenetic profiles, we identified five SNPs potentially affecting enhancer activity in specific tissues. Notably, rs342950505 (SSC1:161,123,588) influences weak enhancer activity across multiple tissues, including the brain. High-throughput chromosome conformation capture (Hi-C) analysis identified that rs342950505 interacts with eight genes. Chromatin state annotations confirmed enhancer activity at this QTL in the cerebellum. Leveraging these insights, single-cell ATAC-seq revealed a chromatin accessibility peak encompassing rs342950505 that regulates PMAIP1 expression in inhibitory neurons via enhancer-mediated mechanisms, with an adjacent peak modulating CCBE1 expression in neuroblasts and granule cells. Transcriptome-wide association studies (TWAS) confirmed PMAIP1's role in the hypothalamus, and Mendelian randomization (MR) validated PMAIP1 and CCBE1 as key brain expression quantitative trait locus (eQTL) effectors. We propose that the variant rs342950505, located within a regulatory peak, modulates PMAIP1 expression in inhibitory neurons, potentially influencing energy homeostasis via hypothalamic regulation. Similarly, CCBE1 may contribute to this process.

Conclusions: Our results, through systematic dissection of pleiotropic BFT-associated loci, provide a framework to elucidate regulatory mechanisms of complex traits, offering insights into polygenic control through lipid metabolism and neural signaling pathways.

Background: Genomic prediction has revolutionized animal breeding, with GBLUP being the most widely used prediction model. In theory, the accuracy of genomic prediction could be improved by incorporating information from QTL. This strategy could be especially beneficial for machine learning models that are able to distinguish informative from uninformative features. The objective of this study was to assess the benefit of incorporating QTL genotypes in GBLUP and machine learning models. This study simulated a selected livestock population where QTL and their effects were known. We used four genomic prediction models, GBLUP, (weighted) 2GBLUP, random forest (RF), and support vector regression (SVR) to predict breeding values of young animals, and considered different scenarios that varied in the proportion of genetic variance explained by the included QTL.

Results: 2GBLUP resulted in the highest accuracy. Its accuracy increased when the included QTL explained up to 80% of the genetic variance, after which the accuracy dropped. With a weighted 2GBLUP model, the accuracy always increased when more QTL were included. Prediction accuracy of GBLUP was consistently higher than SVR, and the accuracy for both models slightly increased with more QTL information included. The RF model resulted in the lowest prediction accuracy, and did not improve by including QTL information.

Conclusions: Our results show that incorporating QTL information in GBLUP and SVR can improve prediction accuracy, but the extent of improvement varies across models. RF had a much lower prediction accuracy than the other models and did not show improvements when QTL information was added. Two possible reasons for this result are that the data structure in our data does not allow RF to fully realize its potential and that RF is not designed well for this particular prediction problem. Our study highlighted the importance of selecting appropriate models for genomic prediction and underscored the potential limitations of machine learning models when applied to genomic prediction in livestock.

Background: Oxidative stress can impair intestinal barrier function and cause liver damage, resulting in reduced animal productivity. Paraquat (PQ) induces significant oxidative stress in weaned piglets. The antioxidant, anti-inflammatory, and metabolic regulatory functions of taurine (Tau), a free amino acid that is widely distributed in the body, have been extensively studied. However, the mechanisms by which dietary Tau alleviates oxidative stress and gut-liver axis damage in weaned piglets remain unclear.

Methods: Forty weaned piglets (20 males and 20 females; 6.41 ± 0.11 kg; 25 days old; Duroc × Landrace × Yorkshire) were used in a 2 × 2 factorial design to investigate the mechanism by which dietary Tau (0% or 0.4%) alleviates PQ-induced oxidative stress and gut-liver axis damage. We analyzed key biomarkers related to gut barrier function, mucosal damage repair, liver damage, gut-liver immunity, antioxidant capacity, systemic immune homeostasis, antioxidant levels, and gut microbiota diversity in piglets under normal and acute oxidative stress. In particular, we evaluated the coordinated regulation of gut-liver axis function mediated by Tau through the Nrf2/Keap1 (antioxidant) and TLR4/NF-κB (immune modulation) signaling pathways. Partial least squares path modeling and molecular docking were used to explore the intrinsic relationship between PQ, Tau, and the gut-liver axis.

Results: PQ exposure impaired gut barrier function, increased the liver fibrosis area, and markedly affected gut microbial diversity (P < 0.05). Tau effectively alleviated PQ-induced oxidative stress by activating the Nrf2/Keap1 pathway and inhibiting the TLR4/NF-κB pathway. This enhanced gut barrier function, promoted mucosal repair, and significantly suppressed the concentration and circulation of lipopolysaccharides in the blood, consequently reducing liver damage (P < 0.05). This further facilitated the optimization of gut microbiota composition, thereby supporting the positive regulation of the gut-liver axis and improving systemic immune and antioxidant functions.

Conclusions: Tau improved the health status of weaned piglets under both normal and stressed conditions by modulating the Nrf2/Keap1 and TLR4/NF-κB pathways, offering a potential new nutritional strategy for alleviating gut-liver damage.

The canine gut microbiome plays a vital role in overall health and well-being by regulating various physiological functions, including digestion, immune responses, energy metabolism, and even behavior and temperament. As such, a comprehensive understanding of the diversity and functional roles of the canine gut microbiome is crucial for maintaining optimal health and well-being. In healthy dogs, the gut microbiome typically consists of a diverse array of bacterial phyla, including Firmicutes, Bacteroidetes, Actinobacteria, Fusobacteria, and Proteobacteria. These microbial communities form a complex ecosystem that interacts with the host to support canine health and homeostasis. A well-balanced microbiome, known as eubiosis, represents an optimized microbial composition that enhances host health and metabolic functions. Eubiosis is shaped by interactions between host physiology and environmental factors. However, dysbiosis, a disruption of eubiosis, can contribute to various health issues, such as weight fluctuations, metabolic disorders, and behavioral changes. Maintaining eubiosis in the canine gut microbiome requires customized management strategies that consider both physiological traits and environmental influences. In this review, we explored the structure and function of the canine gut microbiome, with particular emphasis on its role in health and the key factors that influence and support its maintenance.

Background: Tryptophan is essential for nutrition, immunity and neural activity, but cannot be synthesized endogenously. Certain natural products influence host health by modulating the gut microbiota to promote the production of tryptophan metabolites. Sanguinarine (SAN) enhances broiler immunity, however, its low bioavailability and underlying mechanisms remain unclear. This study aimed to decode the mechanisms by which sanguinarine enhances intestinal immune function in broilers.

Methods: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was employed to identify the main metabolites of sanguinarine in the intestine. Subsequently, equal concentrations of sanguinarine and its metabolites were separately added to the diets. The effects of sanguinarine and its metabolites on the intestinal immune function of broiler chickens were evaluated using 16S rRNA gene amplicon sequencing and tryptophan metabolomics approaches.

Results: We determined that dihydrosanguinarine (DHSA) is the main metabolite of sanguinarine in the intestine. Both compounds increased average daily gain and reduced feed efficiency, thereby improving growth performance. They also enhanced ileal villus height and the villus-to-crypt (V/C) ratio while decreasing crypt depth and upregulating the mRNA expression of tight junction proteins ZO-1, occludin and claudin-1. Furthermore, both compounds promoted the proliferation of intestinal Lactobacillus species, a tryptophan-metabolizing bacterium, stimulated short-chain fatty acid production, and lowered intestinal pH. They regulated tryptophan metabolism by increasing the diversity and content of indole tryptophan metabolites, activating the aryl hydrocarbon receptor (AhR) pathway, and elevating the mRNA levels of CYP1A1, CYP1B1, SLC3A1, IDO2 and TPH1. Inflammatory cytokines IL-1β and IL-6 were inhibited, while anti-inflammatory cytokines IL-10 and IL-22, serum SIgA concentration, and intestinal MUC2 expression were increased. Notably, DHSA exhibited a more pronounced effect on enhancing immune function compared to SAN.

Conclusions: SAN is converted to DHSA in vivo, which increases its bioavailability. DHSA regulates tryptophan metabolism by activating the AhR pathway and modulating immune-related factors through changes in the gut microbiota. Notably, DHSA significantly increases the abundance of Lactobacillus, a key tryptophan-metabolizing bacterium, thereby enhancing intestinal immune function and improving broiler growth performance.

Extensive evidence demonstrates that a healthy and well-balanced gut microbiota profoundly influences host nutrient absorption, immunity, and metabolism. Unlike mammals, early microbiota colonization in commercial poultry largely depends on the environment as chicks hatch in incubators under a relatively sterile environment (egg and incubator sterilization) without maternal-offspring interaction. The early gut microbiota remains unsaturated, providing a critical window for modulation and influencing the subsequent microbiota succession, which may have long-term health outcomes. Microbiota transplantation (MT) involves transferring the microbiota from a donor to a recipient to modulate the recipient's microbiota toward a desired state. Successfully applied in human medicine, MT is also gaining attention in poultry production to modulate intestinal health. This review comprehensively explores factors affecting MT, its mechanisms, and its potential applications in chickens, providing insights for further research and commercial use.

Probiotic extracellular vesicles (pEVs) are biologically active nanoparticle structures that can regulate the intestinal tract through direct or indirect mechanisms. They enhance the intestinal barrier function in livestock and poultry and help alleviate intestinal diseases. The specific effects of pEVs depend on their internal functional components, including nucleic acids, proteins, lipids, and other substances. This paper presents a narrative review of the impact of pEVs on the intestinal barrier across various segments of the intestinal tract, exploring their mechanisms of action while highlighting the limitations of current research. Investigating the mechanisms through which probiotics operate via pEVs could deepen our understanding and provide a theoretical foundation for their application in livestock production.