Front Cell Infect Microbiol. 2026 Aug 26;16:1896940. doi: 10.3389/fcimb.2026.1896940. eCollection 2026.

ABSTRACT

INTRODUCTION: Lawsonia intracellularis causes Porcine Proliferative Enteritis (PPE), leading to significant economic losses, yet obtaining isolates for vaccine development remains challenging.

METHODS: In this study, a novel L. intracellularis strain, designated LIGD01, was isolated from the ileum of a pig with acute hemorrhagic enteritis in Guangdong, China. The strain was stably passaged in McCoy cells for 40 generations.

RESULTS: Phylogenetic analysis of the 16S rRNA gene confirmed its identity, and indirect immunofluorescence assay (IIFA) and scanning electron microscopy (SEM) demonstrated characteristic intracellular colonization and curved rod-shaped morphology. LIGD01 induced intermittent fecal shedding starting at 3 days post-infection (dpi), with seroconversion in all challenged pigs by 21 dpi. Necropsy revealed distinct ileal hyperplasia. Histopathology showed villous blunting, epithelial exfoliation, and inflammatory infiltration. Crucially, infection significantly reduced Average Daily Gain (ADG) (252.21 ± 17.07 g/day vs. 300.98 ± 19.39 g/day in controls, p < 0.05) and suppressed the activities of key digestive enzymes (trypsin, lipase, amylase) in the pancreas and intestine. Furthermore, Lawsonia intracellular infection characterized by a reduction in beneficial genera (Lactobacillus, Christensenellaceae) and an increase in opportunistic pathogens (Streptococcus, Enterococcus), concomitant with upregulated pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1α).

DISCUSSION: This study not only provides a new candidate strain for vaccine development but also elucidates the physiological and microbial mechanisms underlying growth retardation in PPE.

PMID:42718558 | PMC:PMC13553240 | DOI:10.3389/fcimb.2026.1896940

Food Waterborne Parasitol. 2026 Aug 26;44:e00356. doi: 10.1016/j.fawpar.2026.e00356. eCollection 2026 Sep.

ABSTRACT

Parasitic helminths can modulate host inflammatory responses, but whether this regulation involves remodeling of the intestinal neurochemical environment remains unclear. Here, we investigated whether Trichinella spiralis infection alters intestinal neurotransmitter-related metabolism during lipopolysaccharide (LPS)-induced systemic inflammation. In this study, we established an LPS-induced inflammatory model and a T. spiralis-infection with LPS challenge model. At 14 days after infection, mice were challenged with LPS, and inflammatory responses and duodenal neurotransmitter-related metabolites were assessed. T. spiralis infection reduced serum TNF-α and IL-1β levels and alleviated LPS-induced lung pathology. Targeted LC-MS/MS profiling revealed treatment-specific neurochemical signatures in duodenal tissues. Under basal conditions, T. spiralis infection increased histamine levels and reduced norepinephrine, 5-hydroxyindoleacetic acid, and xanthurenic acid. During LPS challenge, prior T. spiralis infection was associated with increased dopamine, epinephrine, levodopa, 5-hydroxytryptophan, histamine, and tyramine compared with LPS challenge alone. These changes suggest that T. spiralis infection remodels tyrosine-, histidine-, and tryptophan-related neurochemical pathways in the intestine. Receiver operating characteristic analysis further identified several metabolites that discriminated LPS-challenged mice from T. spiralis-infected, LPS-challenged mice, although these candidate signatures require validation in larger independent cohorts. Together, our findings indicate that intestinal neurochemical remodeling may represent a previously underappreciated component of helminth-associated anti-inflammatory regulation.

PMID:42713351 | PMC:PMC13551873 | DOI:10.1016/j.fawpar.2026.e00356

Antioxidants (Basel). 2026 Aug 15;15(8):1019. doi: 10.3390/antiox15081019.

ABSTRACT

Superoxide dismutase 2 (SOD2), a key mitochondrial antioxidant enzyme, is essential for maintaining cellular redox homeostasis by scavenging superoxide radicals. While viruses often induce oxidative stress, the specific role of SOD2 in antiviral defense remains unclear. Here, we report that vaccinia virus (VACV) infection triggers mitochondrial and cellular reactive oxygen species (ROS) and selectively upregulates SOD2, but not SOD1. Genetic knockout of SOD2 exacerbated mitochondrial ROS (mtROS) accumulation and significantly enhanced VACV replication and spread, resulting in larger viral plaques. Conversely, SOD2 overexpression constrained plaque formation and suppressed viral dissemination. Mechanistically, the antiviral function of SOD2 does not strictly rely on its enzymatic activity or mitochondrial targeting, as neither the deacetylation-mimicking mutant nor the mutant lacking the mitochondrial localization signal peptide appreciably impaired its antiviral potency. Furthermore, in a rabbit model, local overexpression of human SOD2 attenuated the poxvirus lesion formation. Our findings unveil an important yet easily overlooked role of SOD2 in antiviral defense and posit it as a promising candidate for the development of host-directed therapeutics against poxviruses.

PMID:42650283 | PMC:PMC13509771 | DOI:10.3390/antiox15081019

Hum Vaccin Immunother. 2026 Dec;22(1):2715930. doi: 10.1080/21645515.2026.2715930. Epub 2026 Aug 26.

ABSTRACT

The exchange of knowledge and best practices is essential for improving adult vaccination strategies across the European region. Finland serves as a valuable example, with a centralized, publicly funded National Vaccination Program (NVP) supported by national evaluation for decision-making based on comprehensive population-based registers. These registers enable assessment of disease burden, facilitate the identification of high-risk groups, and enable evaluating vaccination coverage, impact, and safety during the implementation. The NVP allows a centralized tender with lower vaccine prices, centralized vaccine procurement, and uniform processes for vaccine administration by public health care. Despite these strengths, Finland faces challenges in adult vaccination similar to other EU countries, including budgetary constraints, as well as the need for improved implementation, especially for high-risk groups. The complex evaluation, decision, funding, and procurement process causes delays in vaccine introduction into the NVP. This review describes Finland's adult vaccination system, from policy to implementation, drawing on a structured search of PubMed/MEDLINE, gray literature (2009-2024) and expert input. While there are areas for further improvement, Finland's commitment to provide cost-effective, equitable, evidence-based vaccination programs with high coverage, including for at-risk subpopulations, ensures continued progress.

PMID:42647143 | PMC:PMC13523915 | DOI:10.1080/21645515.2026.2715930

Poult Sci. 2026 Jul 27;105(11):107500. doi: 10.1016/j.psj.2026.107500. Online ahead of print.

ABSTRACT

Goose astrovirus (GAstV) is a newly identified avian pathogen that causes fatal gout in goslings, characterized by kidney damage and high mortality. Unlike non-pathogenic human gout, GAstV-induced gout lacks reference models due to the absence of goose-derived cell lines and standard experimental animals, limiting mechanistic studies. Here, primary goose kidney organoids (GKOs) were isolated from 28-day-old goose embryos. GKOs retained physiological structures and functions comparable to in vivo kidneys. GAstV infection in GKOs was evaluated across renal cell lineages and compared with in vivo outcomes. Viral replication and effects on uric acid metabolism were assessed at different multiplicities of infection. GAstV readily infected GKOs, targeting progenitor, pluripotent stem, collecting duct, and renal tubular cells, consistent with in vivo findings. At a multiplicity of infection of 10.0, GAstV rapidly induced a significant elevation of uric acid, whereas lower doses had weaker effects, paralleling disease severity in goslings. In contrast, GAstV replication was minimal in 2D cells, and other avian viruses failed to induce uric acid elevation in GKOs. Post-infection, transcriptomic and metabolomic analysis showed GAstV remodeled global gene expression and metabolism, mainly disrupting purine metabolism pathways. GAstV infection significantly increased mRNA levels of SLC22A23, SLC17A5, and SLC13A3, which were correlated positively with uric acid. GKOs provide a physiologically relevant model for elucidating GAstV pathogenesis, offering new insights into virus-induced gout and a platform for studying goose viral diseases.

PMID:42617253 | PMC:PMC13521225 | DOI:10.1016/j.psj.2026.107500

Vet Res Commun. 2026 Jul 28;50(5):486. doi: 10.1007/s11259-026-11423-w.

ABSTRACT

Since 2022, a decrease in egg production and hatchability, along with hepatitis-like symptoms, has been frequently reported in Muscovy duck farms in southern China. Using metagenomic sequencing, a novel Chaphamaparvovirus (ChPV), designated MuChPV-GD2022, was detected in the livers of the diseased ducks. Phylogenetic analysis revealed that the MuChPV-GD2022 strain shares 61.8-77.4% genome identity with duck-origin Chaphamaparvoviruses, and 44.3-77.4% with avian-origin Chaphamaparvoviruses. The NS1 protein amino acid sequence showed a 29.3-71.5% similarity to those of other known Chaphamaparvoviruses. These findings support the classification of MuChPV-GD2022 as a new species in the genus Chaphamaparvovirus, family Parvoviridae. Since virus isolation was not achieved due to technical constraints, the evidence suggests MuChPV may be associated with the hepatitis-like disease. Furthermore, a TaqMan qPCR assay targeting NS1 gene of the virus was developed and validated for specificity, sensitivity, and repeatability, which provides a sensitive tool not only for virus detection but also for epidemiological surveillance of MuChPV infections.

PMID:42518002 | DOI:10.1007/s11259-026-11423-w

J Ethnopharmacol. 2027 Jan 10;372:122219. doi: 10.1016/j.jep.2026.122219. Epub 2026 Jul 21.

ABSTRACT

ETHNOPHARMACOLOGICAL RELEVANCE: Platycodon grandiflorus (PG) is a traditional herb widely used for respiratory infections. Newcastle disease virus (NDV) is a highly contagious and devastating pathogen that causes severe economic losses to the poultry industry. Platycodin D (PD), a bioactive component of PG, has not been investigated for its antiviral activity against NDV.

AIM OF THE STUDY: We investigated the antiviral activity of PD against NDV and elucidated its underlying host-targeted mechanisms.

MATERIALS AND METHODS: The anti-NDV activity of PD was evaluated in vitro and in vivo. Transcriptomic and network pharmacology were employed to map PD-targeted pathways. Mechanistic dissection was achieved by examining MAPK signaling cascade, NLRP3 inflammasome assembly, inflammatory cytokine profiling, apoptosis regulation, and type I interferon response.

RESULTS: PD significantly inhibited NDV replication in vitro and in vivo, reducing viral loads and tissue injury in infected chickens. Transcriptomic profiling combined with network pharmacology analysis identified inflammation-, apoptosis-, and interferon-related pathways as major targets of PD, with MAPK signaling emerging as a central regulatory node. Mechanistic studies demonstrated that PD suppressed NDV-induced activation of the MAPK pathway and NLRP3 inflammasome assembly, leading to decreased production of pro-inflammatory cytokines (IL-1β, IL-6, IL-8, and IL-18). In parallel, PD attenuated virus-induced apoptosis through upregulation of the anti-apoptotic protein Bcl-2. Moreover, PD enhanced antiviral immunity by promoting IFN-α/β expression and STAT1 phosphorylation.

CONCLUSION: PD restricts NDV infection by coordinately modulating host inflammatory, apoptotic, and innate antiviral signaling pathways, supporting its potential as a host-targeted antiviral candidate for the control of Newcastle disease.

PMID:42480879 | DOI:10.1016/j.jep.2026.122219

BMC Vet Res. 2026 Jul 15. doi: 10.1186/s12917-026-05703-5. Online ahead of print.

ABSTRACT

BACKGROUND: Hepatitis E virus (HEV) is a major zoonotic foodborne pathogen causing human acute hepatitis, with genotype 4 endemic in China and swine as its main reservoir. Guangdong has a large intensive swine industry, yet stratified molecular epidemiological data on swine HEV are lacking. This study explored the prevalence, risk factors and genetic traits of swine HEV in Guangdong to support zoonotic disease control.

METHODS: A total of 1280 pig fecal samples from farms and abattoirs were tested for HEV RNA via RT-nPCR targeting ORF2. All positive samples underwent Sanger sequencing, and partial isolates were amplified for near-full-length genomes. Phylogenetic trees were built using the maximum likelihood method with 1000 bootstraps. Samples were grouped by region, season and sampling site; subgroup detection rates were compared via χ² and Fisher's exact tests, and binary logistic regression identified independent risk factors (P < 0.05).

RESULTS: The overall HEV positive detection rate was 2.66% (34/1280, 95% CI: 1.85-3.69). Detection rates differed markedly by region (P < 0.001) and season (P < 0.05), with no discrepancy between farms and abattoirs (P > 0.05). Region and season were independent risk factors. All isolates were HEV genotype 4, dominated by subtype 4a plus minor 4b and 4d strains, with consistent genotyping results from ORF2 and full-length genomes. Wide genetic divergence existed among local strains, and amino acid mutations concentrated in the ORF1 hypervariable region.

CONCLUSION: Swine HEV prevalent in Guangdong Province mainly belongs to genotype 4 and exhibits obvious regional and seasonal distribution characteristics. Continuous and targeted surveillance in high-risk regions and peak epidemic seasons is recommended to reduce the zoonotic transmission risk of swine HEV and ensure public health safety.

PMID:42458441 | DOI:10.1186/s12917-026-05703-5

Curr Res Food Sci. 2026 May 25;12:101448. doi: 10.1016/j.crfs.2026.101448. eCollection 2026.

ABSTRACT

Chemical disinfectants and bacteriophages for controlling Salmonella in foods often have limitations such as residual odor, narrow antimicrobial spectra, and poor stability under food processing conditions. Lasso peptides, with their structural stability, heat resistance, and safe antimicrobial activity, are promising candidates for food preservation. In this study, Chitosan-Citric acid-MccJ25-MccY (CCJY) nanoparticles were prepared via citric acid crosslinking to encapsulate MccJ25 and MccY. The nanoparticles showed high encapsulation efficiency (>96.67%) and maintained their antimicrobial activity in the presence of food matrices. CCJY exhibited strong anti-Salmonella activity on the surface of eggs and chilled chicken, achieving 99.9% bacterial reduction. Importantly, CCJY retained its efficacy after heat treatment and under acidic/alkaline conditions typical of food processing. In egg preservation, CCJY treatment maintained eggshell integrity (0.82% weight loss, Haugh unit 61.12 after 20 days). In chilled chicken, CCJY reduced total bacterial counts by 2.37 log₁₀ CFU/g and decreased drip loss by 12.5% (p < 0.001), extending shelf life by 3-4 days. These results demonstrate that CCJY is an efficient and safe antimicrobial formulation suitable for application in egg and meat preservation.

PMID:42282865 | PMC:PMC13251780 | DOI:10.1016/j.crfs.2026.101448

Poult Sci. 2026 Aug;105(8):107104. doi: 10.1016/j.psj.2026.107104. Epub 2026 May 9.

ABSTRACT

Avian coccidiosis, especially infection caused by the highly pathogenic Eimeria necatrix, causes major economic loss in the poultry production. With the increasing limitations of anticoccidial drugs and live vaccines, there is an urgent need for novel, broad-spectrum control strategies. In this study, a reverse vaccinology workflow was used to screen the proteomes of five Eimeria species. Six highly conserved membrane protein families were selected: carbonic anhydrase (CA), mechanosensitive ion channel (MSC), cell division control protein 50 (CDC50), major facilitator superfamily transporter (MFS), ATP-binding cassette transporter (ABC) and lipid transfer protein (LTP). Antigenic fragments from these families were linked with EAAAK linkers to generate a chimeric multi-antigen fusion construct, EimeriaBig. Five prime-boost regimens were tested in chickens challenged with E. necatrix. The regimen of one protein prime followed by two DNA boosts showed the highest protection among the tested regimens, with moderate protective efficacy. Our results demonstrated that a heterologous strategy, comprising a recombinant protein prime (rEimeriaBig) followed by two DNA vaccine boosts (pcDNA3.1-EimeriaBig), conferred the best protection among the regimens tested, with moderate efficacy. In this group, cecal lesion score was reduced by 47.64 % and oocyst output was reduced by 49.75 %, and the anticoccidial index was 168.72. The same regimen produced higher antigen-specific IgY and increased transcription of IL-2, IFN-γ, and IL-10. These results support further optimization of this vaccine strategy for control of E. necatrix.

PMID:42214189 | PMC:PMC13241995 | DOI:10.1016/j.psj.2026.107104