The aim of this study was to investigate the regulatory roles of distinct signaling cascades within the death receptor pathway in host cell apoptosis induced by Eimeria tenella (E. tenella); to this end, primary chicken embryo cecal epithelial cell culture, gene silencing, enzyme-linked immunosorbent assay (ELISA), Hoechst-Annexin V/PI apoptosis staining, hematoxylin-eosin (HE) staining, and quantitative real-time polymerase chain reaction (qRT-PCR) were employed. At 4, 24, 72, and 120 h post-inoculation (hpi) with E. tenella sporozoites, the proportion of apoptosis in six treatment groups [Group C, Group T0 (E. tenella infection group), Group T1 (E. tenella + Fas SiRNA), Group T2 (E. tenella + TRAIL SiRNA), Group T3 (E. tenella + TNFR1 SiRNA), and Group T4 (E. tenella + NC SiRNA)] and the dynamic changes in Fas cell surface death receptor (Fas), tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), tumor necrosis factor receptor 1 (TNFR1), TNF receptor-associated death domain (TRADD), Fas-associated death domain (FADD), and death domain-associated protein (Daxx) expression and caspase-8 activity in the cells were determined. The results demonstrated that, from 4 to 120 hpi, the Fas and TNFR1 mRNA expression levels in Group T0's host cells were significantly higher than those in Group C (p < 0.05 or p < 0.01). At 72 and 120 hpi, TRAIL mRNA expression in Group T0's host cells was significantly or highly significantly elevated compared to that in Group C (p < 0.05 or p < 0.01). From 24 to 120 hpi, the expression levels of the FADD and Daxx genes, caspase-8 activity, and apoptotic rates in Group T1's host cells were significantly lower than those in Group T4 (p < 0.05). At 72 and 120 hpi, the FADD expression, caspase-8 activity, and apoptotic rates in Group T2's host cells were significantly reduced relative to Group T4 (p < 0.05). Additionally, at 4 hpi, TRADD gene expression in Group T3's host cells was significantly lower than that in Group T4 (p < 0.05), while the apoptotic rate was significantly higher (p < 0.05). However, from 24 to 120 hpi, the TRADD expression, caspase-8 activity, and apoptotic rates in Group T3's host cells were significantly lower than those in Group T4 (p < 0.05). The results indicated that, in the early stages of E. tenella development, TNFR1 overexpression promoted TRADD mRNA expression, thereby inhibiting the apoptosis of E. tenella host cells. In the middle and late developmental stages of E. tenella, the Fas-FADD, Fas-Daxx, TRAIL-FADD, and TNFR1-TRADD apoptotic pathways were all activated, collectively facilitating host cell apoptosis. The pro-apoptotic effects of these pathways were ranked in descending order, as follows: Fas signaling pathway > TNFR1 signaling pathway > TRAIL signaling pathway.

Aeromonas hydrophila (A. hydrophila) is a ubiquitous aquatic pathogen responsible for devastating outbreaks in aquaculture and an emerging food- and waterborne threat to human health. Rapid and reliable on-site diagnostics are crucial for disease surveillance and food safety. Herein, we report the development of a novel molecularly imprinted polymer (MIP)-based electrochemical biosensor utilizing a screen-printed electrode (SPE) for the rapid (<5 min) detection of A. hydrophila directly in fish tissue homogenates. The integration of methylene blue during the electropolymerization process resulted in highly conductive and stable binding cavities, achieving a low limit of detection (LOD) of 101 CFU/mL with a broad linear range up to 106 CFU/mL. The sensor demonstrated excellent selectivity, exhibiting negligible cross-reactivity with Escherichia coli, Staphylococcus aureus, and Listeria monocytogenes. Furthermore, the platform successfully distinguished infected from healthy Cyprinus carpio samples in clinical field trials. Compared to conventional qPCR and ELISA techniques, this portable, cost-effective, and user-friendly biosensor presents a highly practical alternative for real-time aquaculture biosecurity monitoring and post-harvest food safety assurance.

Shiga toxin-producing Escherichia coli (STEC) poses a severe threat to global public health and food safety, creating an urgent need for rapid and sensitive detection of STEC. Herein, a novel fluorescent immunochromatography test strip (FITS) is reported for the detection of STEC O103 using QDs-loaded dendritic silica spheres (named SQS) as a signal tag. The novel FITS employs a phage tail fiber protein as a superior antibody alternative, which was functionalized on the SQS and demonstrates excellent capability for bacterial recognition and binding. This assay successfully achieves the sensitive detection of STEC O103 (2.2 × 102 CFU/mL) within 12 min, achieving performance comparable to conventional PCR while significantly reducing assay time. More significantly, the results of the FITS in real samples were in good agreement with those from PCR, exhibiting comparable accuracy and reproducibility. Given its rapidity, simplicity, sensitivity, and visual detectability, the proposed FITS stands out as an ideal approach for STEC O103 detection and shows great promise for the early warning and diagnosis of bacterial infections.

Riemerella anatipestifer (R. anatipestifer), a pathogenic bacterium, causes systemic infection in poultry. Although antibiotics can alleviate R. anatipestifer infection, their irrational use has worsened antibiotic resistance, rendering existing drugs less effective against the growing number of multidrug-resistant strains. Treatment with compound Chinese herbal medicines (CCHMs), which show the ability to eliminate pathogens and reduce inflammation in the body, offers a promising alternative for the treatment of bacterial infections. Herein, we characterized a multidrug-resistant R. anatipestifer strain isolated from a duck farm in northern Henan Province. On the basis of the pathological characteristics of the infected ducks, a novel CCHM was developed, and its therapeutic efficacy against R. anatipestifer infection was evaluated alongside a preliminary assessment of the therapeutic mechanism. The results showed that the isolated R. anatipestifer belonged to serotype 1 and was multidrug-resistant. The median lethal dose (LD50) of the strain was approximately 1.89 × 109 CFU/mL. In vitro antibacterial assay revealed that the MIC and MBC of the CCHM against the pathogen were both 0.97 mg/mL. The CCHM killed the bacteria rapidly within hours by disrupting bacterial cell structure and integrity. In vivo therapeutic experiments demonstrated that CCHM treatment cleared the bacteria, ameliorated pathological damage, and increased the survival rate by 30 %. Integrated network pharmacology prediction and experimental validation further showed that CCHM treatment significantly downregulated the expression of the pro-inflammatory cytokines interleukin (IL)-1β, IL-8, IL-17A, IL-17F, IL-22, interferon (IFN)-γ, and signal transducer and activator of transcription 3 (STAT3; P < 0.05). These results confirm that CCHM treatment effectively reduced mortality from R. anatipestifer infection through multiple pathways in ducks, providing an important basis for the development of CCHM as an effective alternative for controlling multidrug-resistant R. anatipestifer infections.

PTEN, a canonical dual-specificity tumor suppressor, plays a pivotal role in regulating diverse physiological and pathological processes, including cell proliferation, apoptosis, and immune responses. Infectious bursal disease virus (IBDV) causes an acute, severe immunosuppressive disease in chickens, inflicting catastrophic economic losses on the poultry industry. Although PTEN has been shown to participate in host immunity, its specific role and underlying mechanism in avian defense against IBDV remain poorly understood. In this study, using chicken DF-1 cells and HD-11 cells as experimental models, we systematically investigated the regulatory effects of PTEN on IBDV replication. Bioinformatics analysis revealed that chicken PTEN shares the highest sequence homology with mallard duck PTEN, possessing highly conserved N-terminal phosphatase, C2, and C-terminal domains, with a widespread subcellular distribution across the cytoplasm, nucleus, and mitochondria. In vitro infection assays demonstrated that IBDV challenge significantly up-regulated both the mRNA and protein levels of PTEN in a time-dependent manner. Furthermore, confocal immunofluorescence microscopy revealed that IBDV infection induced a distinct nuclear translocation of PTEN. Further studies showed that PTEN overexpression markedly suppressed IBDV proliferation in a dose-dependent manner, whereas siRNA-mediated knockdown of endogenous PTEN significantly facilitated viral replication. Mechanistically, PTEN suppressed AKT activation to relieve its inhibitory effect on TBK1, thereby robustly enhancing the transcription of type I interferons and downstream interferon-stimulated genes. Taken together, our findings unveil a novel mechanism by which PTEN restricts IBDV replication via activation of the type I IFN pathway, providing fresh theoretical insights and a potential therapeutic target for the prevention and control of IBDV infection.

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.

IntroductionGalectin-9 is a β-galactoside-binding lectin that functions as a critical pattern recognition receptor (PRR) in the host immune system, initiating immune defense responses by recognizing and binding to pathogen-associated molecular patterns (PAMPs) on the surface of microorganisms. In this study, we identified and characterized a novel galectin-9 cDNA, designated CcGal-9, from Yellow River carp (Cyprinus carpio haematopterus).MethodsThe full-length CcGal-9 cDNA was cloned and sequenced, and its structural features were analyzed. Tissue distribution of CcGal-9 mRNA was examined by quantitative real-time PCR. Expression changes following Aeromonas hydrophila and Staphylococcus aureus infections were evaluated. Recombinant CcGal-9 (rCcGal-9) was expressed in Escherichia coli BL21 (DE3), purified, and assessed for binding to various PAMPs and microorganisms. Agglutination assays and survival experiments were conducted to determine functional roles in immune defense. ResultsThe CcGal-9 cDNA is 963 bp in length and encodes a 320-amino acid protein with two distinct carbohydrate recognition domains (CRDs), characteristic of tandem-repeat type galectins. CcGal-9 mRNA was predominantly expressed in the spleen, testicle, and head kidney, with lower levels in the liver and intestine. Upon bacterial infection, CcGal-9 expression was significantly upregulated in multiple immune-related tissues. Purified rCcGal-9 bound LPS, PGN, mannan, and both Gram-positive and Gram-negative bacteria, and exhibited broad-spectrum agglutination activity. Administration of rCcGal-9 markedly improved the survival rate of carp challenged with A. hydrophila. DiscussionThese findings indicate that CcGal-9 is an important PRR in C. carpio, contributing to immune defense against pathogenic microorganisms through PAMP recognition and microbial agglutination. This study enhances our understanding of galectin-mediated immunity in teleost fish.

Infectious bursal disease (IBD) can result in significant immunosuppression and bursal damage in 3-6 week chickens. To investigate the role of important genes from chicken during IBD virus (IBDV) infection, Jinghong laying hens were used to clarify the pathways of immune response. The transcriptional profiles of cecal tonsil of chickens were performed by high-throughput sequencing at the first day and third day post IBDV infection (dpi) and the transcriptional levels of three immunity-related genes, namely IPMK, TAB3, and ZC3H12A, were confirmed in vitro by qPCR. The results showed that 1731 differential genes were obtained in the IBDV-infected group compared to the control group at 1 dpi. Among these, genes related to 229 immune functions and 15 immune pathways were differentially expressed. 2550 differential genes were obtained at 3 dpi, and genes associated with 289 immunological functions and 14 immune pathways were found to have variable expression. According to the findings of GO and KEGG analyses, IBDV infection triggered numerous immune response processes in the cecal tonsil of chicken, including TGF pathway and MAPK pathway. QPCR results in vitro revealed that the mRNA levels of IPMK, TAB3, and ZC3H12A were decreased at 6 h, and up-regulated as time goes on to 36 h during IBDV infection in HD11 cells. In summary, the results established the groundwork for future research on the relationship between IBDV infection and host immune molecules. Further research contributes to the role of immunity-related genes during IBDV infection and provides the effective prevention and control strategy to viral infection.

ETHNOPHARMACOLOGICAL RELEVANCE:Qingqiao is a traditional Chinese medicine widely used for its heat-clearing, detoxifying, antibacterial, and anti-inflammatory properties. Due to these therapeutic effects, it has been commonly employed in the treatment of intestinal inflammatory disorders in China. AIMS OF THIS STUDY:This study aimed to investigate the therapeutic effects of Qingqiao polyphenols (QP) on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC) and elucidate the underlying mechanisms, particularly the roles of NLRP3 and AIM2 inflammasomes in regulating pyroptosis. METHODS:Using a DSS-induced murine UC model and an in vitro pyroptosis model in J774A.1 macrophages, we evaluated the protective effects of QP and explored its mechanisms of action. RESULTS:QP can significantly reduce the levels of inflammatory factors and oxidative stress in UC mice. Further investigation revealed that QP improve UC symptoms by inhibiting the NLRP3/AIM2 inflammasomes and pyroptosis. Consistent results were observed in in vitro experiments, where QP reduced lactate dehydrogenase (LDH) levels and pyroptosis occurrence in J774A.1 cells. Intriguingly, upon NLRP3 inhibition, we observed a compensatory upregulation of AIM2, accompanied by increased levels of GSDMD, IL-1β, and LDH release, suggesting that AIM2 may drive pyroptosis in the absence of NLRP3. Furthermore, AIM2 overexpression led to elevated GSDMD and IL-1β while significantly downregulating NLRP3 expression, indicating a competitive interaction between NLRP3 and AIM2 in pyroptotic signaling. CONCLUSIONS:We found that QP improve DSS-induced UC by inhibiting NLRP3/AIM2 inflammasome-mediated pyroptosis. Moreover, we uncovered a dynamic crosstalk between NLRP3 and AIM2, where compensatory mechanisms may sustain pyroptosis when one pathway is suppressed.

Newcastle disease, caused by the Newcastle disease virus (NDV) and characterised by rapid onset and high mortality rates, is a highly contagious disease in the poultry industry. Interferons (IFN) play a key role in host defence against NDV, however, the non-structural protein V of NDV can antagonise IFN to facilitate NDV immune escape. DNA methyltransferase (DNMT)3A, an important regulator of IFN signalling molecules, may participate in the process by which the V protein inhibits IFN. Here, we found that NDV and V protein can inhibit DNMT3A expression, and DNMT3A participates in V protein inhibition of IFN expression. Further analysis revealed that the V protein interacts with DNMT3A and promotes its degradation via the K48-ubiquitin pathway. DNMT3A enhances the transcription and expression of IFN-β without altering the methylation status of the IFN-β gene. Instead, DNMT3A reduces the methylation of the CpG island in the IRF7 promoter region and increases the overall CpG island methylation within the IRF7 gene body, thereby increasing IRF7 expression and modulating IFN-β expression. Our study shows that NDV V protein can bind to and degrade DNMT3A, thereby affecting the methylation level of IRF7 and inhibiting IRF7 expression, ultimately leading to decreased IFN-β expression.

Background: Traditional Chinese medicine offers potential therapeutic options for viral infections. Platycodon grandiflorus (PG) is a perennial herb known for its efficacy in treating respiratory infections, including asthma, cough, and bronchitis, making it a key focus in antiviral drug research. The purpose of the study is to provide a basis for functional studies on PG and generate new insights for treating viral diseases. Methods: Research articles from 1990 to 2024 related to PG and viruses were obtained from databases, such as PubMed, Web of Science, and Science Direct, and systematically analysed. Results: PG demonstrates inhibitory effects on viruses such as severe acute respiratory syndrome coronavirus and porcine reproductive and respiratory syndrome virus by blocking various stages of viral proliferation or activating the host immune system. It also reduces inflammation through NF-κB, PI3K/AKT, MAPK, and other signalling pathways, enhancing T cell and macrophage function and increasing host immunity. PG exhibits diverse pharmacological effects with promising clinical applications for antiviral and immune modulation. Given its medicinal significance, PG holds substantial potential for further exploration and development. Conclusion: PG, due to its antiviral, anti-inflammatory, and immune-boosting properties, can be used as an antiviral drug.

Porcine reproductive and respiratory syndrome virus (PRRSV), the causative pathogen of PRRS, remains one of the most important pathogens threatening the global pig industry. Due to the genetic diversity of PRRSV, the existing commercially vaccines cannot completely protect pigs from PRRSV infection. Flavonoid compounds play an important role in inhibiting viral replication. In this study, we found that calycosin, a natural active compound isolated from astragalus, could inhibit PRRSV replication regardless of whether calycosin was added pre-, co-, or post-PRRSV infection in vitro. Furthermore, coincubation of calycosin with PRRSV showed a better inhibitory effect compared to separate incubation, and calycosin mainly inhibited virus replication, assembly and release stages. Importantly, calycosin enhanced the antiviral immunity, as shown by the increased expression of IFN-β and ISG56. Subsequently, we discovered that calycosin promoted the expression of RIG-I and MAVS, and induced the phosphorylation and nuclear translocation of IRF3 during PRRSV infection. Collectively, calycosin could markedly inhibit PRRSV replication and activate the RIG-I/IRF3 signaling pathway. These data contribute to understanding the role of calycosin in PRRSV replication, and may provide valuable insights for the development of future antiviral strategies.

Collectin-11 (CL-11) is a multifunctional lectin that binds carbohydrates on pathogens and inhibits infection through direct neutralization, agglutination, opsonization and killing pathogens, playing an important role in innate immunity. In the present study, a homolog of collectin-11 (CL-11), designated as CcCL-11, was identified and functionally characterized from Yellow River carp (Cyprinus carpio haematopterus). Its expression profile and agglutination activity were systematically analyzed. The full-length cDNA of CcCL-11 was 834 bp and it contained an open reading frame (ORF) of 831 bp that encoded 277 amino acids. The amino acid sequence of CcCL-11 contains signal peptide, collagen-like region (CLR), α-helical neck region and carbohydrate recognition domain (CRD). Tissue expression profiling analysis showed that CcCL-11 was ubiquitously distributed in the tested tissues and was highly expressed in the liver. Furthermore, CcCL-11 expression was significantly upregulated in the liver and intestine after challenge with a Gram-positive bacterial pathogen (Staphylococcus aureus) and a Gram-negative bacterial pathogen (Aeromonas hydrophila). The recombinant CcCL-11 (rCcCL-11) is able to agglutinate and bind to Aeromonas hydrophila, Aeromonas veronii, Escherichia coli, Klebsiella pneumoniae, Micrococcus lysodeikticus, Bacillus subtilis and Staphylococcus aureus and it possessed haemagglutination activity against C. carpio erythrocytes. In addition, rCcCL-11 showed concentration-dependent binding to major bacterial cell wall components such as lipopolysaccharide (‌LPS) and peptidoglycan (PGN). Competition ELISA analysis showed that certain concentrations of carbohydrates can inhibit the binding of rCcCL-11 to bacteria. These findings confirm the biological activity of CcCL-11 and suggest that it plays an important role in pattern recognition. In vivo experiments demonstrated that rCcCL-11 could promote the clearance of A. hydrophila in the liver, kidney, and spleen of C. carpio, and enhance the survival rate of the fish. In summary, the results of this study indicate that CcCL-11 has obvious agglutination and binding effects on pathogenic bacteria and may serve as a pattern recognition receptor (PRR) to participate in the natural immune response of C. carpio against bacterial infection.

Interferon-inducible transmembrane protein 3 (IFITM3), a member of the interferon-stimulating factor (ISG) family, has a wide range of antiviral functions. Infectious bursal disease virus (IBDV) mainly invades the bursa of Fabricius in chickens, causing a reduction in their immunity and resulting in death from secondary infections. Our previous study found that IBDV infection promotes the expression of chicken IFITM3. However, the role of chicken IFITM3 in IBDV infection remains unknown. To explore this role, the overexpression vector for IFITM3 was constructed and transfected into HD-11 and DF-1 cells. The results showed that the overexpression of IFITM3 significantly reduced IBDV proliferation. While the IBDV proliferation increased when IFITM3 was inhibited by using siRNA. To further explore the mechanism by which IFITM3 reduces IBDV proliferation, the effects of IFITM3 on interferon (IFN) were investigated. Transfecting the constructed IFITM3 vectors into HD-11 and DF-1 cells demonstrated that IFITM3 promoted the expression of IFN-α, IFN-β, and IFN-γ. To investigate the mechanism by which IFITM3 regulates IFN expression, the effects of IFITM3 on IFN production were explored. The results showed that the IKB gene mainly affected the regulatory effects of IFITM3 on IFN. Taken together, IFITM3 may reduce viral proliferation by regulating changes in IFNs, and this process may involve a positive feedback effect of IFITM3 on IFN. IKB plays an important role in the regulation of IFN effects by IFITM3.

ADP-ribosylation factor 6 (ARF6) is a small G protein with extensive functions, including regulation of cellular membrane transport and viral infection. Infectious bursal disease (IBD) is caused by infectious bursal disease virus (IBDV), which mainly invades the bursa of Fabricius and causes low immunity in poultry. Our study demonstrated that IBDV infection could promote the expression of ARF6; however, the underlying mechanism remains unclear. Herein, the function of ARF6 in IBDV infection was explored, and it was revealed that viral replication was significantly promoted by ARF6 overexpression and hampered by siRNA-mediated inhibition of ARF6. Using two site mutants of ARF6 (ARF6-T27N and ARF6-Q67L), we found that IBDV replication was repressed by ARF6-T27N, indicating that ARF6 promotes IBDV replication. Further exploration of its mechanism revealed that ARF6 affects the copy number of IBDVs entering cells. A clathrin inhibitor (pitstop 2) impeded the early replication of IBDV, even when ARF6 was overexpressed. These results indicated that ARF6 promotes viral replication by affecting the internalization of IBDV, which may involve clathrin-dependent endocytosis. Our findings improve the understanding of the processes governing IBDV infection and provide insights into its prevention and control.

The literature shows that maternal stress can influence behavior and immune function in F1. Yet, most studies on these are from the laboratory, and replicated studies on the mechanisms by which maternal stress drives individual characteristics are still not fully understood in wild animals. We manipulated high- and low-density parental population density using large-scale field enclosures and examined behavior and immune traits. Within the field enclosures, we assessed anti-keyhole limpet hemocyanin immunoglobulin G (anti-KLH IgG) level, phytohemagglutinin (PHA) responses, hematology, cytokines, the depressive and anxiety-like behaviors and prevalence and intensity of coccidial infection. We then collected brain tissue from juvenile voles born at high or low density, quantified mRNA and protein expression of corticotropin-releasing hormone (CRH) and glucocorticoid receptor gene (NR3C1) and measured DNA methylation at CpG sites in a region that was highly conserved with the prairie vole CRH and NR3C1 promoter. At high density, we found that the F1 had a lower DNA methylation level of CRH and a higher DNA methylation level of NR3C1, which resulted in an increase in the expression levels of the CRH mRNA and protein expression and further reduced the expression levels of the NR3C1 mRNA and protein expression, and ultimately led to have delayed responses to acute immobilization stress. Juvenile voles born at high density also reduced anti-KLH IgG levels and PHA responses, increased cytokines, and depressive and anxiety-like behaviors, and the effects further led to higher coccidial infection. From the perspective of population density inducing the changes in behavior and immunity at the brain level, our results showed a physiological epigenetic mechanism for population self-regulation in voles. Our results indicate that altering the prenatal intrinsic stress environment can fundamentally impact behavior and immunity by DNA methylation of HPA-axis genes and can further drive population fluctuations in wild animals.

Rapid and accurate detection of pathogenic bacteria is crucial for ensuring food safety and public health. In this study, we aimed to develop a novel molecularly imprinted polymer sensor based on screen-printed electrodes for the specific detection of Salmonella typhimurium. The sensor was constructed by electropolymerizing dopamine in the presence of Salmonella typhimurium on the electrode surface, followed by the removal of the bacteria to create specific binding cavities. The sensor demonstrated excellent specificity for Salmonella typhimurium, with a detection limit approximately of 101 CFU/ml and a detection time of only 4 min, with the sensor accurately differentiating Salmonella typhimurium from other common foodborne pathogens such as Escherichia coli and Listeria monocytogenes. The performance of the sensor was validated using real food samples, including pork and milk, showing its well suited for rapid and on-site detection of pathogenic bacteria. The development of this molecularly imprinted polymer with electrochemical sensor represents a significant advancement in the field of electrochemical biosensors, offering a promising tool for food safety monitoring and public health protection.

Chronic hyperglycemia can result in damage to the hippocampus and dysfunction of the blood-brain barrier (BBB), potentially leading to neurological disorders. This study examined the histological structure of the hippocampus and the expression of critical genes associated with the BBB at 2 early stage time points in a streptozotocin-induced diabetes mellitus (DM) mouse model. Routine histology revealed vascular congestion and dilation of Virchow-Robin spaces in the hippocampal CA1 region of the DM group. Neuronal alterations included rounding and swelling and reduction in Nissl bodies and increased apoptosis. Compared to the control group, TJP1 mRNA expression in the DM group was significantly lower (P < .05 or P < .01), while mRNA levels of JAM3, TJP3, CLDN5, CLDN3, and OCLN initially increased and then decreased. At 7, 14, and 21 days, mRNA levels of the receptor for advanced glycation end products (AGER) were greater in the DM group than in the control group (P < .05 or P < .01). These findings indicate that early-stage diabetes may cause structural and functional impairments in hippocampal CA1 in mice. These abnormalities may parallel alterations in the expression of key BBB tight junction molecules and elevated AGER expression in early DM patients.

Artemisia argyi (AA) is promising as a potential feed additive. Microbial fermentation is beneficial to the degradation of cell walls and the better release of bioactive compounds of AA. However, there are few reports on the application of fermented AA as a feed additive for broilers. The present study intended to evaluate the application value of fermented AA as a feed additive for broilers by examining the effects of the dietary supplementation of Aspergillus niger-fermented AA and unfermented AA on growth performance, slaughter performance, and meat quality of brokers. A total of 360 newly hatched (1-day-old) broilers with similar body weight were randomly divided into the following 5 groups: basal diet group as control (C) group, basal diet +3% unfermented AA (E1) group, basal diet + 1% fermented AA (E2) group, basal diet + 3% fermented AA (E3) group, basal diet + 5% fermented AA (E4) group. Each group included 6 replicates with 12 broilers per replicate, and the feeding trail lasted for 48 d. Body weight and feed intake were recorded every 2 wk, and the feed gain ratio was calculated to assess growth performance. At 42 d, 6 broilers from each group were slaughtered, and the carcass traits were calculated. The results showed that compared with the control group, Aspergillus Niger could effectively destroy AA fiber, which contributed to better release of AA bioactive compounds. Moreover, dietary supplementation with AA could improve the growth performance of broilers (P < 0.05), and the effect of fermented AA was better than unfermented AA, especially 3% fermented AA. From 28 to 42 d, compared with the control group, the average daily gain of broilers in the group supplementation with 3% fermented AA was significantly increased (P < 0.05), and the feed-to-gain ratio was decreased (P < 0.05). At 42 d, the dressing percentage, half-eviscerated carcass percentage, eviscerated carcass percentage, and breast muscle percentage of broilers in the groups of 1, 3, and 5% fermented AA diets were significantly improved (P < 0.05), and the thigh muscle percentage of broilers in the group with 3% fermented AA diets was significantly improved (P < 0.05). Meanwhile, the meat quality of broilers in the group with fermented AA diets was also significantly improved. Birds in AA groups had higher a* value and lower shear force of breast muscle, especially the group supplementation with 3% fermented AA (P < 0.05). In conclusion, fermented AA has good application value as a potential feed additive for broilers, dietary supplementation of fermented AA can improve the production performance and meat quality of broiler chickens, of which 3% fermented AA is more effective.