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Intestinal development is a critical determinant of growth and overall health in pigs. Accumulating evidence underscores the significant influence of intestinal microbiota on essential physiological functions and systemic health. Dietary nutrients play a pivotal role in regulating both intestinal development and the composition of intestinal microbiota. Optimal early-life nutrient provision ensures proper intestinal growth and functional maturation, with maternal nutrition emerging as a key factor shaping intestinal development during fetal and neonatal stages. This review synthesizes recent studies on maternal nutrient intake—encompassing protein, energy, carbohydrates, minerals, vitamins, probiotics, and prebiotics—and their effects on intestinal growth and health of offspring. Emerging multi-omics evidence has revealed that gestational and lactational nutrition dynamically coordinates offspring intestinal development through vertical microbial transmission and epigenetic mechanisms, such as DNA methylation and histone acetylation. These processes further regulate intestinal barrier maturation, mucosal immunity, and enteroendocrine signaling. Collectively, this review emphasizes that enhancing maternal nutrition can promote postnatal growth by enhancing intestinal development and early microbial colonization in piglets. Further research is crucial to determining the optimal nutritional strategies during the perinatal period.

Infection with transmissible gastroenteritis virus (TGEV) has been associated with villous atrophy within 48 h, which seriously disrupts intestinal homeostasis. However, the underlying mechanisms remain elusive. In this study, we found that TGEV infection severely disrupted intestinal homeostasis via inhibition of self-renewal and differentiation in Lgr5 intestinal stem cells (ISCs). Profoundly, TGEV-encoded NSP10/NSP16 protein complex-mediated the inactivation of Notch signaling provided a mechanistic explanation for this phenomenon. Initial invasions by TGEV-targeted Paneth cells through aminopeptidase N (APN) receptor, then inducing mitochondrial damage and ROS generation in them, ultimately causing Paneth cell decrease and loss of Notch factors (DII4 and Hes5), which are essential for Lgr5 ISCs self-renewal and differentiation. Interestingly, loss of Notch signaling induced goblet cells differentiation at the cost of absorptive enterocytes and promoted mucins secretion, which accelerated TGEV replication. Therefore, the more differentiation of goblet cells, the greater TGEV infection in jejunum. These results provide a detailed mechanistic pathway by which villous atrophy sharply occurs in TGEV-infected jejunum within 48 h. Thus, the pathogenesis of TGEV can be described as a “bottom up scenario”, which is contrary to the traditional “top down” hypothesis. Together, our findings provide a potential link between diarrheal virus infection and crypt cells response that regulates Paneth cells function and Lgr5 ISCs fate and could be exploited for therapeutic application.

Novel antimicrobial strategies are necessary to tackle using antibiotics during the suckling and weaning period of piglets, often characterized by E . coli -induced diarrhea. In the last decades, acetate, propionate, and butyrate, all short-chain fatty acids (SCFAs), have been proposed as an alternative to antibiotics. SCFAs are instrumental in promoting the proliferation of enterocytes, preserving intestinal integrity, and modulating the microbial community by suppressing the growth of pathogenic bacteria in pigs. The effect of individual SCFAs (proprionate, acetate and butyrate) on the regenerative capacity of intestinal cells was investigated via an optimized wound-healing assay in IPEC-J2 cells, a porcine jejunal epithelial cell line. IPEC-J2 cells proved a good model as they express the free fatty acid receptor 2 (FFAR2), an important SCFA receptor with a high affinity for proprionate. Our study demonstrated that propionate ( p = 0.005) and acetate ( p = 0.037) were more effective in closing the wound than butyrate ( p = 0.190). This holds promise in using SCFA’s per os as an alternative to antibiotics.

Purpose Dietary protein, as important macronutrient, is vital for intestinal function and health status. We aimed to determine the effects of dietary protein source on growth performance and intestinal function of neonates with intrauterine growth retardation (IUGR) in a pig model. Methods Eighteen pairs of IUGR and normal birth weight (NBW) weaned pigs were allotted to be fed starter diet containing soybean protein concentrate (SPC) or spray-dried porcine plasma (SDPP) for 2 weeks. Growth performance, antioxidant variables, intestinal morphology and absorption capability, microbiota composition and short-chain fatty acids (SCFA) were assessed. Results IUGR led to poor growth performance, absorption capability and changes on antioxidant variables, while SDPP diet improved the growth performance, diarrhea index, intestinal morphology and antioxidant variables of IUGR or NBW pigs relative to that fed SPC diet. Importantly, SDPP diet improved bacterial diversity and increased the abundance of phylum Firmicutes , but decreased the phylum Proteobacteria in colonic digesta, associating with higher genera Lactobacillus and lower genera Escherichia – Shigella , linking to the increased concentration of SCFA. Conclusions Our findings indicate that IUGR impairs the growth rate, intestinal function and oxidative status of weaned pigs, which could be partly improved by SDPP diet either for IUGR or NBW pigs, associating with the better antioxidant capability, composition of microbiotas and their metabolites.

Background: Transmissible gastroenteritis virus (TGEV) is a highly pathogenic porcine coronavirus that causes severe gastrointestinal damage in piglets. However, how TGEV affects host iron homeostasis, oxidative stress, and the ferroptosis process remains unclear. This study aimed to investigate the effects of TGEV infection on cellular iron metabolism, oxidative damage, and lipid peroxidation-mediated ferroptosis, as well as to evaluate the potential therapeutic role of retinoic acid (RA). Methods: Using an intestinal epithelial cell model of TGEV infection, we assessed key regulators of iron handling, oxidative stress, lipid peroxidation, and ferroptosis. The expression of ferroportin (FPN) and ferritin (FTH/L) and the activity of the p62–NRF2–GPX4/HO-1 antioxidant axis were analyzed, and the effects of exogenous RA treatment on these endpoints were examined. Results: TGEV infection disrupted cellular iron homeostasis by downregulating the expression of ferroportin (FPN) and ferritin (FTH/L), leading to the accumulation of intracellular free iron, which in turn induced the generation of a large amount of reactive oxygen species (ROS) and ultimately triggered ferroptosis in intestinal epithelial cells. Additionally, TGEV infection significantly inhibited the p62-NRF2-GPX4/HO-1 antioxidant signaling pathway, further exacerbating the ferroptosis process. Conclusions: This study reveals that ferroptosis is a key pathological mechanism in TGEV-induced intestinal injury and demonstrates that RA exerts a therapeutic effect by regulating iron metabolism and activating the p62-NRF2-GPX4/HO-1 signaling pathway. These findings provide new theoretical insights for potential intervention strategies targeting virus infection-associated ferroptosis and intestinal damage.

Long-term nutritional excess causes hepatic steatosis, endoplasmic reticulum (ER) stress, hyperglycemia, and hyperlipidemia. Mitogen-activated protein kinase phosphatase-3 (MKP-3) is a well-established stress-regulated protein and a regulator of gluconeogenesis. Our previous study revealed that acute ER stress reduced gluconeogenesis and MKP-3 protein stability. However, the expression of MKP-3 and its regulatory mechanisms in chronic ER stress remain unclear. The aim of this study was to investigate the effects of chronic ER stress on hepatic MKP-3 expression and its role in the regulation of gluconeogenesis. The results show that long-term administration of thapsigargin (Tg) or palmitic acid promoted gene expression of Mkp-3 and gluconeogenic genes Pepck, G6pc, and Pgc1α in primary mouse hepatocytes. In addition, a long-term high-fat diet (HFD) or Tg administration significantly increased hepatic ER stress and blood glucose level in mice, while inducing the expression of Mkp-3 and hepatic gluconeogenic genes Pepck, G6pc and Pgc1α. Further study revealed that liver-specific Mkp-3 knockout (Mkp-3 LKO) reversed the blood glucose level and expression levels of gluconeogenic genes those were induced by long-term HFD in mice. Moreover, activation of the PKR-like ER kinase (PERK) by its agonist increased hepatic Mkp-3 expression, whereas inhibitor of PERK suppressed the expression of Mkp-3 under Tg administration. These results suggest that chronic high-fat diet might promote hepatic gluconeogenesis via the PERK/MKP-3 pathway. Consequently, this study identified a potential therapeutic target for treating obesity-related hyperglycemia.

This study first adopted a liquid microbial-enzymatic co-fermentation process to enhance the nutritional value of walnut meal (WM) and sesame meal (SM), and systematically evaluated its effect on the nutrient digestibility of growing pigs. WM and SM are two underutilized high-protein by-products, whose application is hindered by anti-nutritional tannin and fiber. Optimal fermentation parameters were determined via single-factor experiments and response surface methodology, utilizing a consortium of Lactobacillus I, Candida utilis, and protease. Fermentation significantly reduced tannin (39.41% in WM) and crude fibre (28.79% in WM), reduced tannin (18.67% in SM) and crude fibre (4.00% in SM), while elevating crude protein (10.63% in WM, 7.47% in SM) and acid-soluble protein in both WM and SM. Results of the microstructure of fermented WM and SM revealed structural loosening, surface porosity, and polysaccharide degradation. Microbial community shifts highlighted the dominance of Lactobacillus and Bacillus in fermented substrates. In growing pigs, fermented WM and SM exhibited improved standardized ileal digestibility (SID) of key amino acids (threonine, tryptophan, valine; p < 0.05), alongside enhanced digestible energy (DE) and metabolizable energy (ME) for SM (p < 0.05). These findings demonstrate that liquid co-fermentation effectively degrades anti-nutritional factors, enhances nutrient bio-availability, and positions WM and SM as viable alternatives to conventional protein sources in swine diets, supporting strategies to reduce reliance on soybean meal.

This study was conducted to investigate the effects of Clostridium butyricum addition to diets in late gestation and lactation on the reproductive performance and gut microbiota for sows. A total of 180 healthy Landrace × Yorkshire sows at 90 d of gestation were randomly assigned to one of four groups, with 45 replicates per group, receiving a basal commercial diet (Control, 0% C. butyricum) or diet added with 0.1% C. butyricum (1 × 108 CFU/kg of feed), 0.2% C. butyricum (2 × 108 CFU/kg of feed), 0.4% C. butyricum (4 × 108 CFU/kg of feed), respectively. The experiment was conducted from 90 d of gestation to weaning at 21 d of lactation. The results showed that the interval between piglet born was linearly (P < 0.05) decreased, and the duration of farrowing was significantly (quadratic, P < 0.05) shortened as C. butyricum addition increased. There was a linear (P < 0.05) increase in litter weight at weaning and litter weight gain. The concentrations of IgG and IgM in colostrum, and IgM in milk were linearly increased (P < 0.05) as C. butyricum addition. Serum MDA concentrations of sows at parturition and 14 d in lactation, and piglets at 14 and 21 d of age were linearly (P < 0.05) decreased, respectively. The serum total antioxidant capacity concentrations of sows at parturition and 14 and 21 d in lactation, and piglets at 14 and 21 d of age were linearly (P < 0.05) increased as C. butyricum addition, respectively. There was a linear decrease in the serum endotoxin concentration of sows on 21 d in lactation (P < 0.05). The serum cortisol concentrations of piglets at 14 and 21 d of age were both significantly (quadratic, P < 0.05) decreased. The 0.2% C. butyricum increased the relative abundance of Bacteroidetes (P = 0.016) at phylum level, Prevotellaceae_NK3B31_group, Prevotella_1, Prevotellaceae_ UCG-003, Prevotella_9, Alloprevotella (P < 0.05) at genus level, and decreased the relative abundance of Proteobacteria, Gemmatimonadetes, Actinobacteria (P < 0.001) at phylum level, and Clostridium_sensu_stricto_1, Streptococcus, Escheruchia-Shigella, Sphingomonas, Succinivibrio (P < 0.05) at genus level and Firmicutes/ Bacteroidetes ratio (P = 0.020). In conclusion, the present research indicated that dietary addition with C. butyricum could shorten the duration of farrowing and enhance the growth performance of suckling piglets. Moreover, 0.2% C. butyricum administration to sows changed the composition of intestinal microbiota, especially increased the relative abundance of Prevotella.

Background This study aimed to investigate the impacts of guar gum and cellulose as the source of dietary fiber during gestation on the reproductive performance of sows. Methods A total of 210 sows (parities 3–6) were randomly allocated into six diets ( n  = 35) throughout gestation to feed graded levels of dietary fiber (DF), including a corn-soybean meal-based control diet with no wheat bran inclusion (CON, 12.5% DF), a wheat bran-rich diet (DF1, 17.4% DF), and another 4 diets (DF2, 17.7% DF; DF3, 18.1% DF; DF4, 18.4% DF; DF5, 18.8% DF) in which wheat bran were equally substituted by 1%, 2%, 3% and 4% purified FIBER MIX (guar gum and cellulose, 1:4). All sows received similar DE and other nutrients throughout gestation. Results DF treatment during gestation resulted in normal fecal score (1 to 5 with 1 = dry and 5 = watery) in sows compared with those received the CON diet ( P  <  0.05). The number of total born piglets had a tendency to be affected by dietary treatment ( P  = 0.07), and correlation analysis revealed a linear response of total born to dietary fiber levels during gestation ( P <  0.01). Sows received the DF2, DF3, and DF5 diets during gestation had a greater ADFI during lactation compared with those in the CON group ( P <  0.05) without affecting the daily body weight gain of suckling piglets. Gut microbiota compositions were dramatically changed by the gestation stage and some of those were changed by DF inclusion. Fecal acetate, propionate, and butyrate of sows were markedly increased in late gestation, and butyrate contents in feces of gestating sows were significantly affected by DF levels ( P <  0.01). Serum concentrations of pro-inflammatory TNF-α were decreased and anti-inflammatory IL-10 was increased on day 30 of gestation by DF levels ( P <  0.05). Conclusions In summary, increasing dietary fiber levels by guar gum and cellulose during gestation improved the reproductive performance of sows, which might be related to changes in immunity and gut microbiota of sows.

Widespread antibiotic use increases the risk of livestock acting as potential reservoirs of antimicrobial resistance genes (ARGs) that may be transferred to human and animal pathogens. Particularly, maternal-infant transmission of antibiotics via breastmilk represents a great concern regarding infant health. In this study, we investigated the effects of 4-week low-dose antibiotic (LDA) treatment on the host immunity and antibiotic resistomes in weaned piglets. Transcriptomic analyses of ileum tissues revealed that the affected genes were largely enriched in innate immunity-related pathways. Significantly reduced protein expression of inflammatory factors, i.e., γ were observed. In addition, analyses of antibiotic resistomes identified a total of 1,021 ARGs related to 39 classes of antibiotics. The samples exhibited highly individual-specific diversity and no significant difference in the structure and diversity of ARGs and mobile gene elements (MGE) after LDA exposure for both colon and ileum samples. Despite of that, there were significant changes in the abundance of two transferrable ARGs [Erm(T) and tcr3] related to the antibiotics administered, implying an increased risk of transferrable antibiotic resistance. There was a significant change in the abundance of one pathogenic species after LDA exposure in the colon samples and one in the ileum samples, but there were no significant differences in the matched ARGs. Collectively, our findings reveal considerable changes in intestinal immunity-related genes, but minimal effects on gut antibiotic resistomes (ARGs and MGEs) in weaned piglets after 4 weeks LDA exposure. Our study provides a foundation for evaluating the longer-term cumulative effects of LDA use, especially the effects of maternal-infant LDA transmission, on antibiotic resistance and risks to infant health.