Journal of Animal Science and Biotechnology最新文献

Background: As probiotics, Bacillus strains may regulate some physiological functions in animals. This study aimed to evaluate whether dietary supplementation with a Bacillus-based probiotic could alleviate gut damage induced by rotavirus (RV) infection in piglets. Twenty-four piglets were randomly assigned into 2 groups fed with the basal diet (n = 16) and the diet containing 10⁹ colony-forming unit Bacillus spores/kg (n = 8). On d 8, 8 piglets fed with the diet supplemented with Bacillus-based probiotic and 8 piglets fed with basal diet were orally infused with RV, while the residue piglets had oral gavage of sterile essential medium. The trial duration was 12 d.

Results: RV challenge induced diarrhea, significantly destroyed the morphology of jejunal mucosa (P < 0.05), significantly increased RV-antibody and RV non-structural protein 4 of jejunal mucosa (P < 0.05), significantly impaired antioxidant capacity (including malondialdehyde level, total antioxidant capacity and catalase activity), immunity (such as interleukin 2, interleukin 4 and secreted immunoglobulin A levels), mucins and the mRNA expression of tight-junction-related (such as Zonula occludens 1, occludin) and apoptotic-related (including B-cell lymphoma/leukaemia-2-associated X protein, B cell lymphoma/leukaemia-2, cysteinyl aspartate specific proteinases) genes of jejunal mucosa (P < 0.05), and, to some extents, affected the bacteria community structure and abundance of ileal digesta in piglets. However, Bacillus-based probiotic administration could significantly attenuate the negative effects of RV infection on gut health of piglets (P < 0.05).

Conclusions: These findings suggested that supplementing Bacillus-based probiotic in the diet could decrease diarrhea rate, and improve gut health in weaned piglets, which was associated with regulating intestinal antioxidant capacity, apoptosis, and microbiota.

Background: Inflammatory bowel disease causes intestinal structural damage, impairs gut function, hinders animal growth and development, and reduces farming efficiency. Previous studies demonstrated that lactate alleviates dextran sulfate sodium (DSS)-induced inflammation and mitigates weight loss by enhancing intestinal barrier functions. However, ‌the mechanisms underlying‌ lactate-mediated protection of the intestinal epithelial barrier ‌remain unclear‌. This study aimed to explore the protective effect of lactate on intestinal barrier damage in colitis piglets and the possible underlying mechanisms through in vivo and in vitro experiments.

Methods: A total of 60 21-day-old weaned female piglets were randomly assigned into three groups based on weight: the control group (basal diet with physiological saline gavage), the DSS group (basal diet with 5% DSS gavage), and the DSS + LA group (2% lactate diet with 5% DSS gavage). There were 10 replicates per treatment, with 2 piglets per replicate. Jejunal morphology was assessed via hematoxylin and eosin staining, while Western blotting quantified the protein levels of proliferation markers, including cluster of differentiation 24 (CD24), cyclin D1, and wingless/integrated (Wnt)/β-catenin signaling components. In vitro, 0.08% DSS and 2-32 mmol/L sodium lactate-treated intestinal porcine epithelial cell line-J2 (IPEC-J2) cells (n = 4) were assessed for viability (Cell Counting Kit-8 assay), apoptosis (flow cytometry), and proliferation parameters, including cell cycle analysis and Leucine-rich repeat-containing G-protein coupled receptor 5 (Lgr5⁺) stem cell quantification.

Results: In vivo, DSS administration induced jejunal villus shortening (P < 0.05), downregulated protein levels of CD24, cyclin D1, casein kinase 1 (CK1), and dishevelled-2 (DVL2) (P < 0.05). In vitro, DSS promoted apoptosis, inhibited proliferation, diminished the Lgr5⁺ cell populations (P < 0.05), and reduced S-phase cell proportions (P < 0.05). Conversely, lactate supplementation ameliorated DSS-induced villus atrophy (P < 0.05), restored CD24, cyclin D1, CK1, and DVL2 protein levels (P < 0.05). Furthermore, in vitro, sodium lactate attenuated DSS-induced apoptosis (P < 0.05), enhanced IPEC-J2 proliferation (P < 0.05), expanded Lgr5⁺ cells (P < 0.05), and increased S-phase progression (P < 0.05).

Conclusions: In summary, lactate ameliorated intestinal barrier damage in DSS-induced colitis by activating the Wnt/β-catenin pathway and restoring the balance between epithelial cell proliferation and apoptosis. This study provides novel mechanistic evidence supporting lactate's therapeutic potential for IBD management.

Gut-brain communication via the peripheral neural network is vital for regulating local digestive function and systemic physiology. Gut microbiota, which produces a wide array of neuroactive compounds, is a critical modulator in this bidirectional dialog. Perturbations in the gut microbiota have been implicated in neurological disorders such as depression and stress. Distinct from humans and other monogastric animals, ruminants possess a unique, microbially dense gastrointestinal compartment, the rumen, that facilitates the digestion of fibrous plant materials. These ruminal microbes are likely key contributors to rumen-brain crosstalk. Unlike certain microbe-derived neuroactive compounds produced in the hindgut that are minimally absorbed and primarily excreted in feces, those generated in rumen can reach the small intestine, where they are largely absorbed and affect central nervous system through systemic regulation in addition to the vagal pathway. Notably, emerging evidence suggests that rumen microbiota dysbiosis under stress is associated with abnormal behavior, altered hormonal and neurotransmitter levels. In this review, we introduce the concept of the rumen-microbiome-brain axis by comparing the anatomical structures and microbial characteristics of the intestine and the rumen, emphasizing the neuroactive potential of rumen microbiome and underlying mechanisms. Advances in this frontier hold tremendous promise to reveal a novel dimension of the gut-microbiome-brain axis, providing transformative opportunities to improve ruminant welfare, productivity, and agricultural sustainability.

Background: The rapid development of intensive layer breeding has intensified odor pollution that must be paid attention to for the green transformation of the industry. This study used Jingfen No.6 laying hens as the model to systematically evaluate the regulatory effect of compound microalgal powder (Chlorella vulgaris:Spirulina platensis:Haematococcus pluvialis = 3:1:1, 1:3:1, 1:1:3) on ammonia (NH₃) emissions from laying hen manure.

Results: Through analysis of the static NH₃ production in manure, it was found that the NH₃ emissions within 24 h in the experimental group with 0.50% compound microalgal powder added were reduced to 6.27-16.84 mg (vs.

Control: 28.29 mg), achieving a 40.47%-77.84% reduction. GC/MS and 16S rRNA sequencing analyses indicated that the compound microalgal powder intervened in the remodeling of the microbial community and nitrogen metabolism network in manure, driving the transformation from inorganic nitrogen to organic nitrogen, mitigated the proliferation of NH₃-producing bacteria (such as Escherichia coli, Klebsiella pneumoniae, Kurthia, and Proteus), and increased the abundance of acid-producing bacteria (such as Leuconostocaceae and Lactobacillaceae). The Spirulina platensis powder group had the best emission reduction effect (reduced by 77.84%), and its mechanism was closely related to the mitigation of Gram-negative bacteria activity by phycocyanin and increased synthesis of aromatic compounds, such as 2,3,5-trimethyl-6-ethylpyrazine.

Conclusions: This study revealed the mechanism by which the compound microalgal powder reduces NH₃ emissions by regulating the proliferation of acid-producing bacteria, reshaping the nitrogen metabolism network, and mitigating the activity of NH₃-producing bacteria, while providing theoretical and data support for the development of environmentally friendly feed.

Background: The deposition of intramuscular fat (IMF) in livestock can enhance the flavor and tenderness of meat products, significantly increasing consumer satisfaction. To achieve this industrial trait, this study investigated the regulatory effects of 20 dietary nutrients on sheep IMF deposition using a 3D organoid culture model.

Results: Key nutrients enhancing angiogenesis, adipocyte differentiation, and lipid accumulation were identified through assessments of capillary sprouts development, mRNA expression, and Oil Red O staining. Vitamins C (VC), E (VE), and K₁ (VK1), guanidinoacetic acid (GAA), leucine (Leu), lysine (Lys), methionine (Met), N-carbamylglutamate (NCG), tryptophan (Trp), α-linolenic acid (ALA), linoleic acid (LA), cis-9, trans-11 conjugated linoleic acid (c9, t11-CLA), acetic acid (HAc), and sodium acetate (NaAc) stimulated while vitamins B₉ (VB9), D (VD), K₂ (VK2), taurine (Tau), and sodium butyrate (NaBu) inhibited angiogenesis (P < 0.05). Furthermore, VC, VE, VK1, VK2, GAA, Leu, NCG, Trp, ALA, LA, and HAc enhanced adipocyte differentiation, with VE, VK1, GAA, Leu, LA, and HAc additionally elevating lipid accumulation (P < 0.05).

Conclusions: Various nutrients play distinct regulatory roles in angiogenesis, adipocyte differentiation, and lipid accumulation. These findings provide a roadmap for further optimizing the production of marbled meat through nutritional intervention in actual livestock breeding production.

Mastitis is one of the most significant diseases affecting the development of the dairy industry and has traditionally been associated with pathogenic infections. However, emerging evidence highlights that ruminal microbial homeostasis also plays a crucial role in the pathogenesis of mastitis. Specifically, cows with mastitis exhibit reduced alpha diversity and altered microbial composition in the rumen. Inducing ruminal dysbiosis through a high-concentrate diet has been shown to trigger mastitis in cows, and transplantation of ruminal microbiota from mastitis-affected cows to recipient mice can induce mastitis in mice. Mechanistically, ruminal dysbiosis increases gastrointestinal inflammation and compromises the integrity of the gastrointestinal barrier, thereby facilitating the translocation of harmful bacterial components, metabolites, and pathobionts into the bloodstream. This disruption impairs blood-milk barrier function, leading to systemic inflammation and the development of mastitis. In this review, we summarize recent advances in understanding how ruminal dysbiosis induces mastitis and explore potential prevention and control strategies targeting the modulation of ruminal microbiota.

Background: The objective of this study was to investigate the impacts of different dietary soybean meal (SBM) levels on jejunal immunity in nursery pigs at different days post-weaning.

Methods: Forty-eight pigs (6.2 ± 0.3 kg), weaned at 21 days of age, were assigned to 2 dietary treatments (n = 12) in a randomized complete block design and fed for 20 or 42 d in 3 phases (10, 10, and 22 d, respectively). The dietary treatments consisted of low and high SBM diets. On d 20 and 42, jejunal mucosa and tissue samples were collected. Treatments were arranged in 2 × 2 factors with dietary SBM levels (low and high SBM diets) and days post-weaning (20 d and 42 d post-weaning).

Results: Pigs fed high SBM diets had greater (P < 0.05) relative abundance (RA) of jejunal Prevotella, tended to have greater (P = 0.091) jejunal IgA, had greater (P < 0.05) crypt depth, and tended to have lower (P = 0.064) villus height to crypt depth ratio (VH:CD) than pigs fed low SBM diets. Pigs at 20 d post-weaning had greater (P < 0.05) RA of jejunal Lactobacillus and had greater (P < 0.05) jejunal IL-8 and protein carbonyl than pigs at 42 d post-weaning. Pigs at 20 d post-weaning tended to have greater (P = 0.090) jejunal IgG, tended to have lower (P = 0.059) jejunal IgA, and had greater (P < 0.05) proportion (%) of Ki-67⁺ cells in the jejunal crypt than pigs at 42 d post-weaning.

Conclusion: Pigs fed high SBM diets showed greater RA of Staphylococcus, a greater immune response, and a decreased VH:CD in the jejunum than pigs fed low SBM diets. Pigs at 20 d post-weaning were more susceptible to jejunal inflammation and intestinal damage than pigs at 42 d post-weaning, but the negative impacts of high SBM diets on jejunal inflammation and intestinal damage were consistent compared to low SBM diets at 20 d and 42 d post-weaning.

Backgroud: Efficient communication between the embryo and the endometrium is essential for the successful establishment and maintenance of pregnancy. Uterine-derived extracellular vesicles (EVs) contribute to embryo-maternal communication, supporting early embryonic development. This study aimed to: (i) compare the protein cargo of uterine fluid EVs (UF-EVs) from CYCLIC and PREGNANT heifers; (ii) characterize the protein profile of conditioned medium (CM)-EVs from endometrial explants cultured alone (EXPL) or co-cultured with five d 7 blastocysts (EXPL + EMB) in vitro; and (iii) compare the EV protein cargo between the in vivo and in vitro models (i.e., EXPL vs. CYCLIC and EXPL + EMB vs. PREGNANT).

Results: We identified 1,459 and 1,752 proteins in the UF-EVs of CYCLIC and PREGNANT heifers, respectively. Among these, 12 were exclusive to CYCLIC, and 18 were exclusive to PREGNANT. Among the 1,329 proteins identified in both groups, 16 were differently abundant; ten were more abundant, and six were less abundant in UF-EVs from PREGNANT heifers. In vivo, the changes in UF-EV protein cargo induced by the presence of a blastocyst were related to inflammatory and immune responses, endometrial receptivity, and support of early embryonic development by promoting cell polarity, cell-cell adhesion, and stem cell differentiation. In vitro, we identified 1,501 proteins in the CM-EVs from EXPL, 1,975 in the CM-EVs from EXPL + EMB, and 82 in the CM-EVs from EMB. Additionally, 50 proteins were unique to EXPL + EMB, and another 33 were differentially abundant due to the synergistic interaction between the embryo and the endometrium. These proteins are involved in embryonic development, regulation of stem cell differentiation, establishment and maintenance of cell polarity, interferon tau (IFNT)-mediated cell signaling, endometrial receptivity, and immune modulation. Although there are qualitative and quantitative differences between in vivo and in vitro-derived EVs, UF-EVs from CYCLIC heifers compared to CM-EVs from EXPL, as well as UF-EVs from PREGNANT heifers compared to CM-EVs from EXPL + EMB shared common proteins.

Conclusions: These findings highlight the pivotal role of EVs in embryo-maternal communication, suggesting that their protein cargo may actively contribute to the modulation of the uterine environment to support early embryonic development. Understanding these molecular interactions could provide valuable insights into the mechanisms of implantation and pregnancy establishment.

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.