This study investigated the effects of proline on intestinal injury in piglets infected with porcine epidemic diarrhea virus (PEDV). Twenty-eight 7-day-old piglets were assigned to four groups: control (CON), proline (Pro), PEDV, and Pro + PEDV. Piglets in the Pro and Pro + PEDV groups received oral proline (500 mg/kg body weight) for 7 days. During the last 3 days, piglets in the PEDV and Pro + PEDV groups were inoculated with PEDV. Under PEDV infection, proline administration increased villus height and the villus height/crypt depth ratio in both the jejunum and ileum, and villus width and villus surface area in the ileum. Proline increased PEDV N protein abundance and interferon β (IFN-β) mRNA level in both intestinal segments, suppressed downstream antiviral genes in infected piglets, but upregulated these genes in the jejunum of uninfected piglets. Proline further increased interleukin 1β (IL-1β) concentrations and the expression of inflammation-related genes in the jejunum of infected piglets. Under PEDV infection, proline increased superoxide dismutase (SOD) activity in serum and jejunum, while reducing jejunal H2O2 concentration. Furthermore, proline downregulated genes related to lipid synthesis and ion transport in the jejunum of infected piglets. Transcriptomic and RT-qPCR analyses supported these findings, indicating that proline enhanced immune defense while suppressing lipid metabolism. In conclusion, proline alleviated PEDV-induced intestinal injury by improving villus morphology and enhancing antiviral and antioxidant defenses. However, it promoted viral replication and inflammation, while suppressing lipid metabolism. The multifaceted effects of proline on PEDV infection indicate its practical use warrants careful consideration.

Porcine epidemic diarrhea virus (PEDV) causes severe intestinal injury and economic losses in the pig industry. Arginine (Arg) promotes barrier repair and immune regulation, but its effects on PEDV-induced damage are unclear. This study aimed to investigate whether Arg could alleviate intestinal injury in PEDV-infected piglets. Thirty-two 7-day-old piglets were randomly divided into four groups: Control, Arg, PEDV, and PEDV+Arg. Piglets in the Arg and PEDV+Arg groups were orally administered 400 mg/kg BW Arg from Day 5 to Day 11. On Day 11, PEDV-infected piglets were orally challenged with the virus at a dosage of 1 × 105.5 TCID₅₀ per individual. On Day 14, tissue samples were collected after slaughter. PEDV infection markedly reduced villus height (VH) in the duodenum, jejunum, and ileum, increased crypt depth (CD), decreased plasma D-xylose concentration, and elevated diamine oxidase (DAO) activity, whereas Arg supplementation restored VH, decreased CD in the duodenum and jejunum, increased D-xylose, and reduced DAO activity. Arg also enhanced villin, occludin, and claudin-1 expression, indicating improved barrier integrity. Interestingly, Arg could promote PEDV replication in the small intestine. However, Arg reduced IL-1β, REG3G, and iNOS expression, while upregulating antiviral genes IFITM3, MX1, and DHX58 in the jejunum. Transcriptomic and proteomic analyses indicated that Arg administration may enhance interferon signaling cascades through the RIG-I-like receptor signaling pathway. In conclusion, our results show that Arg exhibits multifaceted effects upon PEDV infection. Although it increases PEDV replication, Arg could enhance intestinal barrier function, attenuate intestinal inflammatory responses, and alleviate PEDV-induced intestinal injury in piglets.

Porcine epidemic diarrhea (PED) is a severe viral disease caused by the porcine epidemic diarrhea virus (PEDV), leading to huge economic losses in the swine industry. Identifying therapeutic targets has long been a critical challenge in preventing and controlling PED through nutritional interventions. In the present study, 100 seven-day-old crossbred (Duroc × Landrace × Large White) healthy piglets from seven independent trials were selected for the experiment. The transcriptomics, proteomics, and metabolomics analyses were conducted on the small intestine and blood of piglets infected with PEDV, and the combined multiple batches of data were subsequently subjected to integrated analysis. Our findings revealed that PEDV infection significantly affected intestinal cell metabolism, especially lipid metabolism. Among those, sphingolipid and lysophospholipid metabolism could be potential pathways for preventive and therapeutic interventions. Additionally, retinol metabolism, mineral absorption, amino acid metabolism, and pyrimidine metabolism were remarkably altered following PEDV infection. Subsequently, candidate hub genes involved in the core pathways, such as apolipoprotein C3 (APOC3), cytochrome P450 family 3 subfamily A member 22 (CYP3A22), and intestinal alkaline sphingomyelinase (ENPP7), were identified and validated. In conclusion, the present study suggests that PEDV infection leads to the reprogramming of enterocyte lipid metabolism. Furthermore, manipulating lipid metabolism may influence the outcome of viral infection, highlighting potential targets for preventive and therapeutic interventions in managing viral infections. IMPORTANCE:Porcine epidemic diarrhea (PED) is a severe viral disease caused by the porcine epidemic diarrhea virus (PEDV), leading to huge economic losses in the swine industry. Identifying therapeutic targets has long been a critical challenge in preventing and controlling PED through nutritional interventions. The present study suggests that PEDV infection leads to the reprogramming of enterocyte lipid metabolism. Furthermore, manipulating lipid metabolism may influence the outcome of viral infection. The study also highlights potential targets for preventive and therapeutic interventions in managing viral infections.

This study investigated the protective effects of glyceryl monooleate (GM) against porcine epidemic diarrhea virus (PEDV)-induced intestinal injury in neonatal piglets. In vitro assays revealed that GM inhibited PEDV replication. Twenty-four seven-day-old piglets were assigned to four groups: control, GM, PEDV, and PEDV + GM. Piglets received 100 mg/kg GM from days 4–10 and were challenged with 10⁶ TCID50 PEDV on day 8. Samples collected on day 11 were analyzed for intestinal morphology, oxidative stress, inflammation, and microbiota composition. PEDV infection significantly impaired growth performance and disrupted intestinal integrity, as shown by reduced villus height, increased crypt depth, and decreased plasma D-xylose levels (P < 0.05). It also induced oxidative stress, elevated plasma malondialdehyde (MDA), hydrogen peroxide (H2O2), and myeloperoxidase (MPO) levels, and activated inflammatory responses through the TNF-α signaling pathway, increasing interferon regulatory factor 7 (IRF7), myxovirus resistance protein 1 (MX1), interferon-stimulated gene 15 (ISG15), and tumor necrosis factor-α (TNF-α) expression (P < 0.05). Gut microbiota analysis revealed an increased abundance of Fusobacterium, Collinsella, and Campylobacter, and a reduction in Bacteroidetes and Allelobacterium (P < 0.05). GM supplementation alleviated PEDV-induced intestinal injury by improving villus height, reducing crypt depth, and enhancing antioxidant capacity through increased catalase (CAT) and total superoxide dismutase (T-SOD) activities (P < 0.05). It also suppressed viral replication and inflammatory signaling, downregulating TNF-α–related genes and cytokines (IRF7, MX1, ISG15, 2’-5’-oligoadenylate synthetase like (OASL), TNF-α, and CXCligand2 (CXCL2) expression, and plasma interleukin-1β (IL-1β) and TNF-α concentrations), and restored microbial balance by reducing pathogenic bacteria such as Escherichia coli and Shigella (P < 0.05). Collectively, these results indicate that GM protects against PEDV-induced intestinal damage by inhibiting viral replication, enhancing antioxidant defenses, modulating inflammatory pathways, and maintaining gut microbial homeostasis.

The protective effect of Compound terminalia chebula extract (HL) against colonic injury induced by Porcine epidemic diarrhea virus (PEDV) infection in neonatal piglets remains unclear. This study aimed to evaluate the mitigating effects of HL on PEDV-induced colonic injury and elucidate the underlying mechanisms. Eighteen 7-day-old Duroc × Landrace × Large White piglets (2.58 ± 0.05 kg) were randomly assigned to three groups (n = 6/group): CON (blank control), PEDV (infected), and HL + PEDV (HL-supplemented + infected). The 11-day trial included 3 days of acclimatization (days 0-3) and an 8-day experimental period (days 4-11). HL (10 mg/kg BW) was orally administered daily to the HL + PEDV group. On day 8, PEDV and HL + PEDV groups were challenged with 3 mL PEDV (3 × 106 TCID50/mL), while CON received Dulbecco's Modified Eagle Medium (DMEM). All piglets were euthanized on day 11 for colonic tissue collection. Results indicated that PEDV infection induced colonic injury, manifested by a significant increase in crypt depth and disruption of intestinal homeostasis. This was evidenced by impaired barrier integrity (upregulation of matrix metalloproteinase-7 gene [MMP7] and matrix metalloproteinase 13 gene [MMP13], mucus disorganization (elevation of mucin 5AC gene [MUC5AC]), oxidative stress (reduced catalase [CAT] activity and increased malondialdehyde [MDA] levels in serum and colon), and inflammation (upregulation of regenerative islet-derived protein 3γ gene [REG3G], S100 calcium-binding protein A8/A9 gene [S100A8/A9], and interleukin-1β gene [IL-1β]). Additionally, PEDV impaired colonic ion transport by downregulating calcium channel genes (Transient Receptor Potential Cation Channel Subfamily V Member 6 gene [TRPV6], Transient Receptor Potential Cation Channel Subfamily M Member 6 gene [TRPM6]). Notably, HL supplementation effectively reversed these adverse effects. HL restored colonic morphology, increased CAT activity, reduced MDA accumulation, and suppressed inflammatory gene expression. Furthermore, HL modulated the expression of genes involved in water and ion transport upregulating Aquaporin 7 gene (AQP7), Chloride Channel Accessory 4 gene (CLCA4), Sodium-Hydrogen Exchanger 3 gene (NHE3), Transient Receptor Potential Vanilloid 6 (TRPV6), and Transient Receptor Potential Melastatin 6 gene (TRPM6) and significantly inhibited PEDV replication, as indicated by the downregulation of the transcription levels of PEDV membranegene (M), nucleocapsid gene (N), and spike gene (S). Taken together, HL alleviates PEDV-triggered colonic tissue damage in suckling piglets via improving colonic antioxidant capacity, mitigating inflammatory response, partially regulating intestinal barrier and ion/water transport-related genes, and downregulating the transcription of PEDV structural genes at molecular and histological levels.

The preventive effect of leucine (Leu) against colonic damage in piglets infected with porcine epidemic diarrhea virus (PEDV) was examined in this study. Three groups (n = 6) were randomly assigned to eighteen 7-day-old Du-roc x Landrace x Large piglets (body weight [BW] = 2.58 +/- 0.05 kg): Control, PEDV-infected (PEDV), and Leu-supplemented + PEDV-infected (Leu + PEDV). Following a three-day period of acclimatization, the Leu + PEDV group was given Leu (400 mg/kg BW) orally every day. On day eight, the PEDV and Leu + PEDV groups were challenged with PEDV, while the Control group was given Dulbecco's Modified Eagle's Medium. Colonic tissues were collected on day 11. PEDV infection induced severe colonic damage by an increase in crypt, disrupting intestinal homeostasis, including impaired barrier integrity (matrix metalloproteinase-7 and matrix metalloproteinase-13 upregulation), mucus disorganization (mucin 5AC elevation), oxidative stress (reduced catalase activity and increased malondialdehyde levels), inflammation, electrolyte imbalance and enhanced viral replication. Leu supplementation reversed these injuries by alleviating oxidative stress, suppressing inflammation, inhibiting viral replication and stabilizing ion homeostasis. This study provides a scientific basis for Leu as a nutritional intervention to alleviate PEDV-induced colonic damage in piglets.

Porcine epidemic diarrhea virus (PEDV) imposes substantial economic losses on the global swine industry owing to its high pathogenicity and transmissibility. Although arginine (Arg) is known to support the integrity of intestinal barrier, it is not clear whether Arg can alleviate intestinal injury induced by PEDV. A total of 32 healthy 7-day-old piglets were randomly assigned to four groups (Control, Arg, PEDV, PEDV + Arg; eight replicates per group). From day 5, piglets in the Arg and PEDV + Arg groups were orally administered Arg at 400 mg/kg body weight until day 11; then, PEDV (1 × 105.5 TCID50) was given orally for two PEDV-infected groups. On day 14, all piglets were slaughtered to obtain blood and intestine samples for further analysis. The results showed that PEDV infection significantly reduced T-SOD and CAT activities in plasma and intestine while elevating MPO levels. Arg supplementation restored T-SOD (plasma, duodenum, ileum), CAT (plasma, ileum), and GSH-Px (jejunum, ileum) activities and reduced MDA (jejunum) content in PEDV-infected piglets. Hematological analysis showed Arg alleviated PEDV-induced increases in MCV and RDW-SD, and significantly elevated MCHC. The real-time quantitative PCR analysis demonstrated that Arg further enhanced PEDV structural genes (M, N, S) expression in the duodenum, ileum, and colon. Concurrently, Arg significantly up-regulated interferon-stimulated genes (MX1, OASL, ISG15, IFITM3) in the ileum, IRF7 in the duodenum and colon, and IFN-β in the ileum. Arg also down-regulated the pro-inflammatory cytokines IL-6 and CXCL2 and the antimicrobial peptide REG3G in the colon, while up-regulating the tissue repair gene MMP13 in the ileum. In conclusion, oral Arg exhibits a unique dual role: it promotes PEDV replication to a certain extent while significantly enhancing antioxidant capacity, strengthening intestinal antiviral immunity, and attenuating intestinal inflammation. These findings highlight Arg’s role in promoting disease tolerance and offer a novel perspective for nutritional intervention strategies against PEDV infection.

Porcine epidemic diarrhea virus (PEDV) is a major pathogen causing severe diarrhea and intestinal damage in piglets. Monolaurin (GML) and tributyrin (TB) are well-documented functional lipids with intestinal health benefits, but their combined efficacy against PEDV infection remains unclear. The present study first investigated the anti-PEDV effect of GML, TB, and their mixtures using PEDV-infected Vero cells. Then, the effects of a microencapsulated TB-GML complex (PE) were evaluated in PEDV-infected piglets, focusing on its protective mechanisms. Vero cells were simultaneously treated with PEDV and graded concentrations of GML (20-40 μmol/L), TB (0.25-0.50 mmol/L), or their combinations to determine for synergistic antiviral effects. In vivo, a total of 30 piglets (2.49 ± 0.38 kg), 7-d-old, were randomly assigned to three groups: negative control (NC), PEDV, and PE + PEDV. After a 3-d adaptation period, piglets in the PE + PEDV group received an oral dose of PE at 100 mg/kg body weight for 7 consecutive days. On d 8, piglets in the PEDV and PE + PEDV groups were orally inoculated with 1 × 106 50% tissue culture infective dose (TCID50) of PEDV per piglet. The experiment lasted for 11 d. The results showed that 40 μmol/L GML alone, or 0.25 mmol/L TB combined with 20-40 μmol/L GML, suppressed virus replication (P = 0.023). The PE administration improved villus morphology and increased expression of genes involved in water and ion transport in the jejunum, including AQP10, KCNJ13, NHE2, and NHE3 (P < 0.05). Additionally, PE reduced serum interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) levels, and downregulated jejunal relative mRNA expression of inflammation-related genes, mainly IL-8, IL-1β, and CXCL2 (P < 0.05). The PE reversed the enhanced antioxidant stress response in the jejunum by reducing total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and myeloperoxidase (MPO) activities (P < 0.05). The PE inhibited PEDV replication, downregulated relative mRNA expression of IFN-β and its downstream genes, and reduced protein abundance of PEDV-N (P < 0.05). Transcriptomic and quantitative real-time PCR (RT-qPCR) analyses revealed that PE restored lipid metabolic homeostasis by balancing lipogenesis, lipid transport, and fatty acid β-oxidation. Moreover, PE increased the abundance of Proteobacteria, Bacteroidota, Bacteroides, and Halomonas, while decreasing the abundance of Firmicutes and Lactobacillus. In conclusion, PE mitigated inflammation, enhanced antioxidant and antiviral capacities, while alleviating disruptions in water and ion transport, lipid metabolism, and gut microbiota.

Poultry farming increasingly seek effective antibiotic alternatives to maintain intestinal health and prevent inflammation, making the identification of safe and functional plant-derived additives of great importance. This study investigated the potential of catechu powder (CP), a polyphenol-rich plant extract, as an antibiotic alternative to modulate intestinal inflammation, barrier function and antioxidant capacity in broiler chickens. One hundred one-day-old Ross 308 broilers were randomly assigned to either a control or CP supplemented group (1,000 mg/kg), with five replicates of 10 birds each. After the feeding trial reached day 27, growth performance was assessed as scheduled. On day 29, two birds per replicate were injected with lipopolysaccharide (LPS, 1 mg/kg BW), while two others received saline. Samples were collected 3 h post-injection for further analyses. The experimental setup was a 2 × 2 factorial arrangements and the interactions between CP and LPS challenge were evaluated, and significant interactions were separated using Tukey's test. The results demonstrated significant interactions (P < 0.05) between dietary CP treatment and LPS challenge with respect to inflammatory response, oxidative stress status, jejunal histomorphology and jejunal barrier functions. Specifically, under LPS challenge, broiler chickens fed a CP-supplemented diet attenuated LPS-induced inflammatory by downregulating gene expressions of duodenal interferon-γ (IFN-γ) by 37% and tumor necrosis factor-α (TNF-α) by 31%, jejunal IFN-γ by 24%, and serum interleukin-8 (IL-8) by 70% and TNF-α by 78% (P < 0.05). Additionally, under LPS challenge, broiler chickens fed a CP-supplemented diet mitigated LPS-induced oxidative stress by reducing concentrations of hydrogen peroxide (H2O2) by 53% and malondialdehyde (MDA) by 30% in the serum, duodenal H2O2 by 54%, and jejunal MDA by 39% (P < 0.05). Furthermore, under LPS challenge, broiler chickens fed a CP-supplemented diet restored intestinal barrier integrity by increasing jejunal villus height by 24% and upregulating gene expressions of jejunal Claudin1 by 52% and Mucin2 by 123% (P < 0.05). In conclusion, dietary CP effectively alleviated LPS-induced immunological stress and intestinal injury in broiler chickens by suppressing inflammatory responses and oxidative damage, thereby supporting its potential as a functional feed additive and a potential candidate for antibiotic replacement.

The impact of ZnO as a feed additive on growth-performance and intestinal function of Enterotoxigenic Escherichia coli (ETEC) K88-infected piglets remains unclear. Fecal scores of piglets in ETEC group were significantly increased compared to control group. ETEC K88 significantly damages the small intestine, including a reduction in villus height in the jejunum, duodenum, and ileum, and a decrease in total superoxide dismutase activity in the jejunum and catalase activity in the ileum and jejunum. Compared to control group, ETEC K88 infection significantly elevated the mRNA level of gene IL-1β and the level of ileal epithelial cell apoptosis. ZnO administration significantly alleviated these negative effects and improved the antioxidative capability of the ileum. Moreover, ZnO supplementation alleviated the imbalance of gut microbiota by restoring the reduced amount of Enterococcus and Lactobacillus in the jejunum, Clostridium in the ileum, and Lactobacillus in the cecum, as well as the increased amount of total eubacteria in the ileum and Enterococcus in the cecum induced by the ETEC K88 infection. In conclusion, ZnO administration can reduce the diarrhea of piglets infected with ETEC K88 by reducing the structural damage of the intestine, attenuating intestinal oxidative stress and epithelial cell apoptosis, and modulating the gut microbiota.

This study aimed to investigate the effects of naringin (NG) on growth performance, antioxidant status, intestinal barrier function, and immune stress in broilers challenged with lipopolysaccharide (LPS). A total of 144 one-day-old Ross 308 broiler chicks were randomly allocated into 2 treatment groups, with six replicates per group and 12 birds per replicate. The groups consisted of a control group (fed a basal diet) and an NG group (fed the basal diet supplemented with 200 mg/kg NG). The trial lasted 21 days; to evaluate the impact of NG on the late-stage growth performance of broilers, the rearing trial continued until 35 days. Body weight was recorded on days 21 and 35 to evaluate growth performance. A 2 × 2 factorial design was implemented in which broilers were challenged with or without LPS, and their diets were supplemented with or without NG. On day 21, two birds per replicate were intraperitoneally injected with 0.5 mg/kg body weight (BW) LPS, while another two birds received an equal volume of saline, in each group of 12 birds. Birds were slaughtered 3 h post-injection for sample collection. Dietary NG supplementation had no significant effect on growth performance (p > 0.05). However, NG markedly improved plasma liver function markers following LPS challenge (p < 0.05). NG significantly increased hepatic glutathione peroxidase (GSH-Px) activity, duodenal and ileal catalase (CAT) activity, and ileal GSH-Px activity (p < 0.05) while reducing malondialdehyde (MDA) levels in the liver, duodenum, jejunum, and ileum, as well as hydrogen peroxide (H2O2) levels in the jejunum and ileum (p < 0.05). Dietary NG supplementation significantly upregulated the relative mRNA expression of Toll-like receptor 4 (TLR4) and interferon-gamma (IFN-γ) in the liver (p < 0.05) and attenuated the LPS-induced upregulation of tumor necrosis factor-alpha (TNF-α) mRNA expression in the jejunum (p < 0.05). NG reduced serum diamine oxidase (DAO) levels (p < 0.05), increased villus height in the duodenum and jejunum (p < 0.05), and increased the villus-height-to-crypt-depth (VH/CD) ratio in the jejunum (p < 0.05). Moreover, NG markedly upregulated the relative mRNA expression of zonula occludens-1 (ZO-1) and occludin in the duodenum while drastically downregulating the relative expression of mucin-2 in the duodenum and ileum (p < 0.05). NG further reduced mucin-2 expression in the jejunum and mitigated the LPS-induced downregulation of ZO-1 in the ileum (p < 0.05). In addition, NG significantly upregulated the expression of X-linked inhibitor of apoptosis protein (XIAP) and B-cell lymphoma 2 (Bcl-2) and downregulated the expression of matrix metalloproteinase-13 (MMP-13) in the liver of LPS-challenged broilers (p < 0.05). Conclusions: Dietary NG supplementation alleviated LPS-induced intestinal and hepatic injury in broilers. NG attenuated the adverse effects of LPS challenge on intestinal barrier function and enhanced antioxidant capacity in broilers by modulating intestinal tight junction expression and antioxidant enzyme activity. NG may serve as a promising eco-friendly additive to enhance resilience against immune stress in broilers.

The present study aimed to explore the effects of dietary phloretin (PT) on growth performance, immune response, and intestinal function in broilers with necrotic enteritis (NE). A total of 288 1-day-old Arbor Acres chicks were assigned to 3 groups, with 8 replicates per group and 12 chicks per replicate. Over 6 weeks, birds were fed a basal diet or the same diet supplemented with 200 mg/kg phloretin. Birds in the challenged groups were inoculated with coccildia during d 7 to 9 and Clostridium perfringens(CP) during d 14 to 18. Results showed that CP and coccidia challenge reduced the average daily gain and average daily feed intake, increased the feed conversion ratio of broilers, induced inflammation and oxidative stress, and inhibited mRNA expression levels for genes associated with intestinal barrier and nutrient transporters (P < 0.05). PT addition to the feed improved growth performance at early phase improved intestinal morphology, and elevated antioxidant capacity via increasing the activity of total antioxidant capacity and superoxide dismutase in the ileum in broilers with necrotic enteritis (P < 0.01). Dietary PT regulated the intesetinal immune function as observed by the increases in the content of secretory IgA in the ileum and decreased cytokines (Interleukin-1β, Interleukin-10) (P < 0.05). Moreover, NE infection significantly disrupted the balance of intestinal flora, and led to a lower level of short-chain fatty acids such as butyric acid concentration in the ileum, while PT improved the microbiota structure, and increased the intestinal acetic acid and butyric acid concentration (P < 0.001). Furthermore, metabolomics analysis indicated PT treatment improve plant secondary metabolites contents like phloretin 2'-o-glucuronide. Additionally, we observed a significant positive correlation among PT, Ligilactobacillus and butyric acid, and a positive correlation between Ligilactobacillus and plant secondary metabolites. Overall, PT supplementation could improve growth performance and ameliorate intestinal injury in broilers with necrotic enteritis by enhancing the antioxidant capacity and immune function, regulating intestinal flora structure and producing plant secondary metabolites.

This study aimed to assess whether dietary supplementation with probiotics could alleviate intestinal injury in lipopolysaccharide (LPS)-challenged piglets. Healthy weaned piglets were randomly allocated to four individual groups (n = 6): (1) a control group; (2) an LPS group; (3) an LPS + Lactobacillus group; and (4) an LPS + Bacillus group. The control and LPS groups received a basal diet, while the probiotic groups were provided with the same basal diet supplemented with 6 × 106 cfu/g of Lactobacillus casei (L. casei) or a combination of Bacillus subtilis (B. subtilis) and Bacillus licheniformis (B. licheniformis) at a dosage of 3 × 106 cfu/g, respectively. On day 31 of the trial, overnight-fasted piglets were killed following the administration of either LPS or 0.9% NaCl solution. Blood samples and intestinal tissues were obtained for further analysis several hours later. The results indicate that dietary supplementation with probiotics significantly exhibited health-promoting effects compared with the control group and effectively reduced LPS-induced histomorphological damage to the small intestine, impairments in barrier function, and dysregulated immune responses via modulation of enzyme activity and the expression of relevant genes, such as nuclear factor-kappa B (NF-κB), interleukin 4 (IL-4), interleukin 6 (IL-6), interleukin 10 (IL-10), claudin-1, nuclear-associatedantigenki-67 (Ki-67), and β-defensins-1 (pBD-1). Collectively, these results suggest that dietary supplementation with probiotics could alleviate LPS-induced intestinal injury by enhancing the immunity and anti-inflammatory responses in piglets. Our research provides a theoretical basis for the rational application of probiotics in the future.

Porcine epidemic diarrhea virus (PEDV) infection poses a significant challenge to the swine industry, with limited effective control measures available. Poria cocos polysaccharides (PCP) is the primary active ingredient of Poria cocos, and has been demonstrated to show beneficial effects on intestinal damage in previous studies. However, its mechanism has not been fully understood. In the present study, 18 seven-day-old piglets were divided into 3 groups: Control group, PEDV group, and PCP + PEDV group. After three days of adaptation, piglets in the PCP + PEDV group were orally administered 10 mg/kg body weight/d PCP from d 4 to 10. On d 8, piglets were orally administered with PEDV at the dose of 104.5 TCID50/piglet. This study aimed to investigate the potential effects of PCP on PEDV-induced intestinal injury and explored the underlying mechanisms. The results showed that PCP administration effectively alleviated diarrhea, reduced PEDV replication in the small intestine and colon of piglets, and significantly improved intestinal mucosal morphology. Specifically, PCP increased the villus height in both the jejunum and ileum and increased the villus height to crypt depth ratio in the ileum (P < 0.05). Improved intestinal function was further evidenced by elevated plasma D-xylose levels and decreased diamine oxidase activity (P < 0.05). Transcriptomic and proteomic analyses revealed that lipid metabolism is a key pathway regulated by PCP during PEDV infection. Notably, PCP significantly upregulated sphingolipid metabolism-related genes, including ectonucleotide pyrophosphatase/phosphodiesterase family member 7 and N-acylsphingosine amidohydrolase 2. Metabolomic analysis revealed that PCP primarily modulated the levels of plasmanylphosphoethanolamine, lysophosphatidylcholine, and carnitine. Additionally, PCP reversed the expression of key genes involved in fatty acid uptake, intracellular lipid transport, and fatty acid synthesis, such as fatty acid binding protein 2, fatty acid transport protein 4, apolipoprotein B, apolipoprotein C3, fatty acid synthase, long-chain fatty acyl CoA synthetase 3, lipoprotein lipase and acyl-CoA thioesterases 12 (P < 0.05). These findings demonstrate that PCP mitigates PEDV-induced intestinal injury by modulating lipid metabolism and highlight its potential as a dietary supplement for enhancing anti-PEDV defenses and promoting intestinal health in piglets.

This study investigated the protective effects of glycerol monooleate (GMO) against porcine epidemic diarrhea virus (PEDV)-induced intestinal injury in neonatal piglets. Twenty-four 7-day-old piglets were divided into four groups: CTRL, GMO, PEDV, and PEDV + GMO. From D 4–10, piglets in GMO groups received 100 mg/kg GMO supplementation. Piglets in PEDV–infected groups were challenged with 10⁶ TCID₅₀ PEDV per piglet on D 8. Blood and intestinal samples were collected from all piglets after euthanasia on D 11 to assess intestinal morphology, oxidative stress status, inflammatory response, and intestinal microbiota. PEDV infection significantly reduced average daily gain (ADG) during D 9–11 ( P < 0.05), impaired intestinal barrier function indicated by lower plasma D-xylose, increased duodenal crypt depth (CD) and decreased villus height (VH) and VH/CD ratios in duodenum, jejunum, and ileum. PEDV caused oxidative stress, elevating plasma and duodenum malondialdehyde (MDA) content, plasma hydrogen peroxide (H₂O₂) content, and myeloperoxidase (MPO) activity, while duodenum catalase (CAT) activity declined ( P < 0.05). PEDV activated systemic inflammation through TNF-α signaling pathway, indicated by upregulating IRF7 , MX1 , IFN-β , OASL , ISG15 , TNF-α , and CXCL2 mRNA, and elevating plasma IL-1β and TNF-α contents ( P < 0.05). Gut microbiota analysis revealed PEDV increased abundance of Fusobacterium , Collinsella , and Campylobacterota while reducing Bacteroidetes and Alloprevotella ( P < 0.05). GMO supplementation attenuated PEDV-induced intestinal injury, indicated by increasing ileal VH, reducing duodenum and ileum CD, and therefore improving ADG ( P < 0.05). GMO enhanced antioxidant capacity via increasing CAT in plasma and total superoxide dismutase (T-SOD) activities in duodenum and suppressing MDA in ileum and H₂O₂ levels in plasma and jejunum ( P < 0.05). GMO inhibited viral replication and modulated TNF-α signaling pathway, downregulating IRF7 , MX1 , ISG15 , OASL , TNF-α , and CXCL2 expression, reducing plasma IL-1β and TNF-α concentrations ( P < 0.05). In addition, GMO suppressed abundance of pathogenic bacteria such as Escherichia coli and Shigella spp ( P < 0.05). These findings demonstrate that GMO inhibits PEDV replication and alleviates PEDV-induced intestinal damage through multifaceted mechanisms: enhancing antioxidant capacity, mitigating inflammatory responses via TNF pathway regulation, and balancing gut microbiota.

The study investigated the effects of the rearing system and carcase weight on the meat quality of Nero d’Aspromonte pigs. Thirty-three barrows, aged between 14 and 16 months with an average slaughter body weight of approximately 140 and 160 kg, were randomly selected among 80 pigs reared with two different rearing systems, indoor or plein air. Carcase weight was recorded and dressing percentage was calculated. Longissimus thoracis (LT) muscles were sampled and grouped into: plein air and low carcase weight; plein air and high carcase weight; indoor and low carcase weight; indoor and high carcase weight. Proximate composition, cholesterol, vitamin E and fatty acid composition in LT muscles were examined. Rearing systems did not affect carcase yield. However, a higher carcase yield was found for heavier pigs reared indoor compared to lighter pigs reared in plein air system. Neither the rearing system nor the carcase weight affected the proximate composition, cholesterol and vitamin E contents. Meat from plein air reared pigs had higher total saturated fatty acids (SFA) and lower total polyunsaturated fatty acids (PUFA), resulting in a lower PUFA/SFA ratio and n-6 to n-3 PUFA ratio. The combination of the plein air system and heavier carcase weight could improve the nutritional properties of intramuscular fat in this native pig. In conclusion, obtained results indicate that the Nero d’Aspromonte pig is an interesting genetic type that, when reared in the open air and producing heavier carcases, could provide meat more suitable from the nutritional perspective.

The poor intestinal health induced by management, stress, or infection remains a substantial challenge restricting the rapid development of the pig industry. Some natural plant bioactive components (NPBCs) have garnered considerable interest owing to their multifarious benefits, including enhancing intestinal morphology, digestion and absorption, barrier function, immune function, and regulating the gut microbiota. However, there are critical factors, such as the lack of standardized production technologies, lower stability and bioavailability, and unclear mechanisms of NPBCs, severely limiting their feeding efficacy and their application in animal production. Here, we conducted a comprehensive review of the recent advances regarding the impacts of NPBCs on pig gut health. Additionally, we highlighted the key areas that warrant further in-depth investigation. Taken together, NPBCs could be green, safe, and effective feed additives by constructively overcoming their limitations, and they are expected to have broader applications in animal husbandry.

Since 2010, new outbreaks of porcine epidemic diarrhea (PED) caused by porcine epidemic diarrhea virus (PEDV) variant strains have brought significant economic losses to world pig industry. In this study, we isolated a PEDV strain from a new PED outbreak farm in 2024. The strain was identified through RT-PCR, indirect immunofluorescence assay and purified through plaque assay. This virus showed high adaptability to Vero cell during the process of passage and named as HB-2024. Phylogenetic analysis of the S gene showed that the HB-2024 strain was clustered into G2b subgroup. Amino sequence analysis showed that the S protein of the HB-2024 strain had a unique character beside the N terminal of the fusion peptide, which might lead to its high adaptability to Vero cell. We also performed a piglet infection experiment to test its pathogenicity. All piglets infected with this virus showed obvious diarrhea and their small intestines showed serious pathological damage. These results suggest that the HB-2024 strain is a G2b subtype variant that adapts well to Vero cell and can be used to study the adaptive mechanisms of PEDV.