The objective of this study was to investigate the protective effect of Crataegus pinnatifida polysaccharide (CPP) on non-alcoholic fatty liver disease (NAFLD) induced by a high-fat diet (HFD) in mice. The findings demonstrated that CPP improved free fatty acid (FFA)-induced lipid accumulation in HepG2 cells and effectively reduced liver steatosis and epididymal fat weight in NAFLD mice, as well as decreased serum levels of TG, TC, AST, ALT, and LDL-C. Furthermore, CPP exhibited inhibitory effects on the expression of fatty acid synthesis genes FASN and ACC while activating the expression of fatty acid oxidation genes CPT1A and PPARα. Additionally, CPP reversed disturbances in intestinal microbiota composition caused by HFD consumption. CPP decreased the firmicutes/Bacteroidetes ratio, increased Akkermansia abundance, and elevated levels of total short-chain fatty acid (SCFA) content specifically butyric acid and acetic acid. Our results concluded that CPP may intervene in the development of NAFLD by regulating of intes-tinal microbiota imbalance and SCFAs production. Our study highlights that CPP has a potential to modulate lipid-related pathways via alterations to gut microbiome composition thereby ex-erting inhibitory effects on obesity and NAFLD development.

Pseudorabies virus (PRV) infection leads to viral encephalitis and neurological damage in mice, causing significant neurological symptoms and brain damage. This study aimed to investigate the cellular mechanisms of PRV-induced encephalopathy and the role of matrix metalloproteinase-9 (MMP-9) in blood–brain barrier (BBB) disruption. We found that PRV infection increased the number of astrocytes and induced a phenotypic shift from the A2 to the A1 subtype, which was associated with increased secretion of MMP-9. MMP-9 was identified as a critical mediator of PRV-induced BBB disruption, as it degrades collagen VI, leading to BBB damage. PRV was shown to penetrate the BBB via a paracellular pathway, and MMP-9 deletion reversed this damage, mitigating tight junction injury. Additionally, PRV infection caused an “inflammatory storm” in the central nervous system (CNS), with increased levels of the chemokines CCL-3, CCL-4, and CCL-5; the cytokines IL-6 and IL-18; and TNF-α. The expression of INF-γ was significantly decreased. In conclusion, PRV infection disrupts the BBB and induces an inflammatory response in the CNS, with MMP-9 playing a key role in mediating BBB damage. These findings provide insights into the pathogenesis of PRV-induced encephalopathy and potential therapeutic targets for viral encephalitis.

Porcine epidemic diarrhea virus (PEDV) is a highly contagious pathogen responsible for devastating enteric disease and lethal watery diarrhea, leading to significant economic losses in the global swine industry. Understanding the epidemiology and genetic diversity of PEDV over the past decade is crucial for the effective prevention and treatment of porcine epidemic diarrhea. In this study, 1851 fecal samples were collected from pigs exhibiting diarrhea symptoms across 11 cities in Yunnan Province between 2013 and 2022. The prevalence of PEDV, along with other common swine diarrhea viruses, including porcine transmissible gastroenteritis virus (TGEV), porcine rotavirus (PoRV), porcine Sapporo virus (PoSaV), porcine stellate virus (PaStV), and porcine delta coronavirus (PDCoV) was assessed using a polymerase chain reaction (PCR) assay. The results revealed a total detection rate of 52.94% (980/1851) for the six viruses, with PEDV accounting for 25.93% (480/1851) of cases. Further analysis showed that weaned piglets were more susceptible to PEDV than fattening pigs, with the highest prevalence observed in spring (61.52%, 275/447) and the lowest in summer (12.68%, 97/765). Dual infections were also identified, with PEDV + PoSaV being the most common combination (2.81%, 52/1851), followed by PEDV + PoRV, with a detection rate of 1.67% (31/1851). Phylogenetic analysis of the PEDV S genes revealed that the 28 epidemic strains in Yunnan Province shared a nucleotide sequence homology from 91.4% to 98.4% and an amino acid sequence homology ranging from 85.6% to 99.3%. All strains were classified as GII variant strains. This study provides a comprehensive overview of the epidemiology of PEDV and its co-infection patterns with other common diarrhea-causing viruses in the swine herds of Yunnan Province over the past decade. These findings offer valuable insights for the development of effective prevention and control strategies to mitigate the impact of PEDV and other enteroviruses on the swine industry in Yunnan Province.

Porcine pseudorabies has long existed in China and is a serious threat to the Chinese farming industry. To understand the prevalence and genetic variation of the porcine pseudorabies virus (PRV) and its pathogenicity in Yunnan Province, China, we collected 560 serum samples across seven Yunnan Province regions from 2020 to 2021 and detected anti-gE antibodies in these samples. Sixty-one clinical tissue samples were also collected from pigs with suspected PRV that were vaccinated with Bartha-K61. PRV-gE antibodies were found in 29.6% (166/560) of the serum samples. The PRV positivity rate in clinical tissue samples was 13.1% (8/61). Two isolates, PRV-KM and PRV-QJ, were obtained. The identity of the gB, gD, and gE genes between these isolates and the Chinese mutants exceeded 99.5%. These isolates and the classical Fa strain were used to infect 4-week-old rats intranasally to assess their pathogenicity. All infected rats showed the typical clinical and pathological features of PRV two days post-infection. The viral loads in the organs differed significantly among the infected groups. Viruses were detected in the saliva and feces at 12 h. Significant dynamic changes in total white blood cell counts (WBC), lymphocyte counts (Lym), and neutrophil counts (Gran) occurred in the blood of the infected groups at 24 and 48 h. These results show that mutant PRV strains are prevalent in Bartha-K61-vaccinated pigs in Yunnan Province, China. Moreover, rats shed PRV in their saliva and feces during early infection, indicating the need for rodent control in combatting PRV infections in Yunnan Province, China.

Aim of the study: This study aimed to evaluate the protective effects of Glycyrrhiza polysaccharides (GPs) on Pseudorabies virus (PRV)-infected mice and elucidate their mechanisms of action, with a focus on intestinal immunity, oxidative stress, mucosal barrier function, and gut microbiota composition.Materials and methods: GPs were extracted via hot water extraction and ethanol precipitation. Seventy-two SPF-grade male mice were randomly divided into six groups and treated with different doses of GPs or Astragalus polysaccharides (APS), followed by PRV challenge. Clinical parameters, inflammatory cytokines (TNF-α, IL-6, IL-4, IL-10), oxidative stress markers (SOD, CAT, MDA), histopathology, tight junction protein expression (Occludin, ZO-1), sIgA levels, intestinal permeability, viral load, and gut microbiota profiles were assessed.Results: GP administration significantly alleviated PRV-induced symptoms, reduced mortality and disease activity index, and improved food intake. Medium and high doses notably downregulated TNF-α and IL-6, while upregulating IL-4 and IL-10. Antioxidant activities (SOD, CAT) were enhanced, and MDA levels were decreased. Histological analyses showed recovery from villus atrophy and goblet cell loss. GPs improved tight junction integrity, elevated sIgA, reduced gut permeability and viral burden. Microbiota analysis revealed increased α-diversity, enrichment of Lactobacillus and Bacteroides, and suppression of potential pathogens. Functional predictions suggested GPs influenced immunity- and metabolism-related microbial pathways.Conclusion: GPs exert protective effects against PRV-induced intestinal injury by modulating immune and oxidative responses, enhancing mucosal barrier integrity, and rebalancing gut microbiota. These findings support the potential of GPs as a therapeutic agent for viral enteric diseases. To our knowledge, this is the first study to demonstrate the protective role of GPs against PRV infection in vivo. These findings expand current understanding of the antiviral potential of plant-derived polysaccharides and highlight GPs as a promising candidate for the development of novel polysaccharide-based therapeutics for viral enteric diseases.

Background: The global dissemination of multidrug-resistant (MDR) Salmonella poses a persistent and serious threat to food safety systems. As a leading poultry-exporting country, Thailand requires a comprehensive understanding of how resistance plasmids spread among Salmonella populations within its chicken production chain. Methods: Between March 2023 and February 2024, 223 Salmonella isolates were collected from chicken slaughterhouses and markets in northeastern Thailand. From these, 19 representative MDR Salmonella enterica isolates, selected based on distinct spatiotemporal distributions, underwent whole-genome sequencing. Genomic analyses included sequence typing, core-genome phylogenetics, and screening for antimicrobial resistance genes. Plasmid replicons were identified, and functional annotation was performed using the COG database. Results: Phylogenetic analysis revealed 11 distinct sequence types within the population. Among these, ST1541 and ST50 showed clear evidence of clonal transmission across different production stages, with a notable clustering pattern observed during the winter season. All sequenced isolates exhibited an MDR phenotype. Plasmids were detected in 78.9% of isolates, with conjugative plasmids being the most frequent type (57.9%). The β-lactamase gene bla_TEM-60 was the most prevalent (78.9%) and showed a strong correlation (r ≥ 0.7) with resistance to both ampicillin and cefotaxime. Functional annotation further revealed an abundance of genes involved in carbohydrate and amino acid metabolism across all isolates. Conclusions: These findings indicate that MDR Salmonella dissemination is driven by two synergistic mechanisms: the clonal expansion of fit lineages and the horizontal transfer of conjugative plasmids harboring β-lactamase genes. We identified IncI-gamma-K1 and Col-related plasmids as key vectors in this process. This study advocates for targeted interventions, guided by a One Health approach, that specifically aim to disrupt plasmid transmission at critical control points, such as slaughterhouses, to curb the spread of antimicrobial resistance.