Preparation and characterization of nisin-loaded chitosan nanoparticles functionalized with DNase I for the removal of Listeria monocytogenes biofilms.

Listeria monocytogenes biofilms represent a continuous source of contamination, leading to serious food safety concerns and economic losses. This study aims to develop novel nisin-loaded chitosan nanoparticles (CSNPs) functionalized with DNase I and evaluate its antibiofilm activity against L. monocytogenes on food contact surfaces. Nisin-loaded CSNPs (CS-N) were first prepared by ionic cross-linking, and DNase I was covalently grafted on the surface (DNase-CS-N). The NPs were subsequently characterized by Zetasizer Nano, transmission electron microscopy, Fourier transform infrared (FT-IR), and X-ray diffraction (XRD). The antibiofilm activity of NPs was evaluated against L. monocytogenes on polyurethane (PU). The DNase-CS-N was fabricated and characterized with quality attributes (particle size-427.0 ± 15.1 nm, polydispersity [PDI]-0.114 ± 0.034, zeta potential-+52.5 ± 0.2 mV, encapsulation efficiency-46.5% ± 3.6%, DNase conjugate rate-70.4% ± 0.2). FT-IR and XRD verified the loading of nisin and binding of DNase I with chitosan. The DNase-CS-N caused a 3 log colony-forming unit (CFU)/cm2 reduction of L. monocytogenes biofilm cells, significantly higher than those in CSNPs (1.4 log), CS-N (1.8 log), and CS-N in combination with DNase I (2.2 log) treatment groups. In conclusion, nisin-loaded CSNPs functionalized with DNase I were successfully prepared and characterized with smooth surface and nearly spherical shape, high surface positive charge, and good stability, which is effective to eradicate L. monocytogenes biofilm cells on food contact surfaces, exhibiting great potential as antibiofilm agents in food industry. PRACTICAL APPLICATION: Listeria monocytogenes biofilms are a common safety hazard in food processing. In this study, novel nanoparticles were successfully constructed and are expected to be a promising antibiofilm agent in the food industry.

Acid modified attapulgite loaded with bacillomycin D for mold inhibition and mycotoxin removal.

Molds and mycotoxins pose severe threats to health. Bacillomycin D (BD) can effectively inhibit mold growth. Attapulgite (ATP) can provide a good carrier for antimicrobial agents. Natural ATP was acid-modified to obtain H-ATP. It was used to load BD to obtain a novel composite material (H-ATP-BD). The results showed H-ATP had better adsorption performance than ATP. BD was adsorbed up to 93.13 % by adding 30 mg H-ATP and stirring at 40 ℃ for 120 min. Fourier transform infrared spectra (FTIR), size and zeta potential, X-ray diffraction (XRD), and X-ray photoelectron spectroscopy (XPS) results confirmed successful loading of BD onto H-ATP. The composite showed good inhibition of Aspergillus and adding 0.6 % H-ATP-BD composite was effective in removing 89.06 % of aflatoxin B1 (AFB1) at 50 °C. Model fitting indicated that AFB1 removal was a spontaneous exothermic reaction. This research will lay the foundation for the development of efficient and green antimicrobial and toxin-reducing materials.

Broccoli Improves Lipid Metabolism and Intestinal Flora in Mice with Type 2 Diabetes Induced by HFD and STZ Diet.

Globally, type 2 diabetes (T2DM) is on the rise. Maintaining a healthy diet is crucial for both treating and preventing T2DM.As a common vegetable in daily diet, broccoli has antioxidant, anti-inflammatory and anticarcoma physiological activities. We developed a mouse model of type 2 diabetes and carried out a systematic investigation to clarify the function of broccoli in reducing T2DM symptoms and controlling intestinal flora. The findings demonstrated that broccoli could successfully lower fasting blood glucose (FBG), lessen insulin resistance, regulate lipid metabolism, lower the levels of TC, TG, LDL-C, and MDA, stop the expression of IL-1ß and IL-6, and decrease the harm that diabetes causes to the pancreas, liver, fat, and other organs and tissues. Furthermore, broccoli altered the intestinal flora's makeup in mice with T2DM. At the genus level, the relative abundance of Allobaculum decreased, and that of Odoribacter and Oscillospira increased; At the family level, the relative abundances of Odoribacteraceae, Rikenellaceae and S24-7 decreased, while the relative abundances of Erysipelotrichaceae and Rikenellaceae increased.

In-Field Tobacco Leaf Maturity Detection with an Enhanced MobileNetV1: Incorporating a Feature Pyramid Network and Attention Mechanism.

The maturity of tobacco leaves plays a decisive role in tobacco production, affecting the quality of the leaves and production control. Traditional recognition of tobacco leaf maturity primarily relies on manual observation and judgment, which is not only inefficient but also susceptible to subjective interference. Particularly in complex field environments, there is limited research on in situ field maturity recognition of tobacco leaves, making maturity recognition a significant challenge. In response to this problem, this study proposed a MobileNetV1 model combined with a Feature Pyramid Network (FPN) and attention mechanism for in situ field maturity recognition of tobacco leaves. By introducing the FPN structure, the model fully exploits multi-scale features and, in combination with Spatial Attention and SE attention mechanisms, further enhances the expression ability of feature map channel features. The experimental results show that this model, with a size of 13.7 M and FPS of 128.12, performed outstandingly well on the task of field maturity recognition of tobacco leaves, achieving an accuracy of 96.3%, superior to classical models such as VGG16, VGG19, ResNet50, and EfficientNetB0, while maintaining excellent computational efficiency and small memory footprint. Experiments were conducted involving noise perturbations, changes in environmental brightness, and occlusions to validate the model's robustness in dealing with the complex environments that may be encountered in actual applications. Finally, the Score-CAM algorithm was used for result visualization. Heatmaps showed that the vein and color variations of the leaves provide key feature information for maturity recognition. This indirectly validates the importance of leaf texture and color features in maturity recognition and, to some extent, enhances the credibility of the model. The model proposed in this study maintains high performance while having low storage requirements and computational complexity, making it significant for in situ field maturity recognition of tobacco leaves.

Effects of Different Molecular Weight Oxidized Dextran as Crosslinkers on Stability and Antioxidant Capacity of Curcumin-Loaded Nanoparticles.

Curcumin is a polyphenolic compound that has been widely investigated for its health benefits. However, the clinical relevance of curcumin is limited due to its low water solubility and inefficient absorption. Therefore, curcumin is often encapsulated in nanocarriers to improve its delivery and function. In this study, composite nanoparticles composed of stearic acid-modified chitosan (SA-CS) and sodium caseinate (NaCas) were formed using sodium periodate-oxidized dextran with different molecular weights as a crosslinking agent. The effects of oxidized dextran (Odex) with different molecular weights on the composite nanoparticles were compared. The optimal SA-CS/NaCas/Odex composite nanoparticle (NPO) was obtained using an Odex (150 kDa)-to-SA-CS mass ratio of 2:1. Its size, polydispersity index (PDI), and zeta potential (ZP) were 130.2 nm, 0.149, and 25.4 mV, respectively. The particles were highly stable in simulated gastric fluid (SGF) in vitro, and their size and PDI were 172.3 nm and 0.263, respectively. The encapsulation rate of NPO loaded with curcumin (Cur-NPO) was 93% under optimal ultrasonic conditions. Compared with free curcumin, the sustained release of Cur-NPO significantly reduced to 17.9%, and free-radical-scavenging ability improved to 78.7%. In general, the optimal prepared NPO exhibited good GI stability and has potential applications in the formulation of orally bioactive hydrophobic drugs.

Antiobesity effect of L-arabinose via ameliorating insulin resistance and modulating gut microbiota in obese mice.

OBJECTIVES: The global prevalence of obesity, a chronically trophic metabolic disease, has garnered significant attention. The aim of this study was to investigate L-arabinose, a unique functional sugar that improves insulin resistance and intestinal environment while promoting probiotic proliferation, for its potential in preventing obesity induced by a high-fat and high-sugar (HFHS) diet in mice. METHODS: The L-arabinose group was intragastrically administered with 0.4 mL 60 mg/(kg body weight) L-arabinose for 8 wk. The metformin group was intragastrically administered at 0.4 mL 300 mg/(kg body weight), as a positive control group. RESULTS: Treatment with L-arabinose resulted in a reduction of various obesity symptoms, such as prevented weight gain, increased liver-to-body ratio, decreased insulin, homeostasis model assessment for insulin resistance (HOMA-IR) index, and lipopolysaccharide (LPS) levels, as well as improved insulin resistance, reduced fat volume, inhibited hepatic steatosis, and repaired the pancreas. The L-arabinose treatment also improved lipid metabolism and inflammatory response, decreased the Firmicutes-to-Bacteroidetes ratio at the phylum level, and increased the relative abundance of Parabacteroides gordonii and Akkermansia muciniphila at the species level. CONCLUSION: Based on these results, L-arabinose could be a promising candidate for combating obesity and obesity-related diseases by regulating insulin resistance and gut microbiota.

Transcriptomic analysis reveals that Bacillomycin D-C16 induces multiple pathways of disease resistance in cherry tomato.

BACKGROUND: Bacillomycin D-C16 can induce resistance in cherry tomato against pathogens; however, the underlying molecular mechanism is poorly understood. Here, the effect of Bacillomycin D-C16 on induction of disease resistance in cherry tomato was investigated using a transcriptomic analysis. RESULTS: Transcriptomic analysis revealed a series of obvious enrichment pathways. Bacillomycin D-C16 induced phenylpropanoid biosynthesis pathways and activated the synthesis of defense-related metabolites including phenolic acids and lignin. Moreover, Bacillomycin D-C16 triggered a defense response through both hormone signal transduction and plant-pathogen interactions pathways, and increased the transcription of several transcription factors (e.g., AP2/ERF, WRKY and MYB). These transcription factors might contribute to the further activated the expression of defense-related genes (PR1, PR10 and CHI) and stimulated the accumulation of H2O2. CONCLUSION: Bacillomycin D-C16 can induce resistance in cherry tomato by activating the phenylpropanoid biosynthesis pathway, hormone signal transduction pathway and plant-pathogen interactions pathway, thus activating comprehensive defense reaction against pathogen invasion. These results provided a new insight into the bio-preservation of cherry tomato by the Bacillomycin D-C16.

Ingestion of Lacticaseibacillus rhamnosus Fmb14 prevents depression-like behavior and brain neural activity via the microbiota-gut-brain axis in colitis mice.

Large preclinical evidence suggested that colitis was one of the risk factors for depression and probiotics were effective therapeutic agents to prevent the disease. The effect of Lacticaseibacillus rhamnosus Fmb14 on colitis-related depression-like behavior and its possible mechanisms were investigated. One week of DSS exposure led to the following changes in male C57BL/6N mice: a reduction in the movement distance from 2218 to 1299 cm, time in central areas from 23.6 s to 11.5 s, and time in the bright box from 217 s to 103 s, which were restored to 1816 cm, 18.4 s, and 181 s, respectively, with preadministration of Fmb14 for 8 weeks. All improvements provided by Fmb14 indicated a remarkable protective effect on depression-like behavior. Fmb14 first worked to repair intestinal barrier damage and the inflammatory response in the colon through ZO1 and Ocln enhancement and IL-1ß, NF-κB and IL-6 reduction, respectively. Second, dysbiosis of the gut microbiota was modulated by Fmb14, including reduction of Akkermansia (18.9% to 5.4%), Mucispirillum (0.6% to 0.1%) and Bifidobacterium (0.32% to 0.03%). Fmb14 supplementation ameliorates the brain inflammatory response via IL-18 and NF-κB reduction and improves the blood-brain barrier via increased levels of ZO1 and Ocln. Moreover, brain activity was facilitated by an increase in BDNF and dopamine and the downregulation of GABA in the Fmb14 group. As a consequence of the modulatory effect on the dysfunction of neurotransmitters and neuroinflammation, Fmb14 prevents neurodegeneration by inhibiting neuronal apoptosis and Nissl edema. In addition, the correlation analysis further demonstrated the preventative effect of Fmb14 on depression-like behavior through the microbiota-gut-brain axis. Together, these findings demonstrated the important role of Fmb14 in biological signal transduction over the microbiota-gut-brain axis to improve mood disorders.

Surfactin Mitigates Dextran Sodium Sulfate-Induced Colitis and Behavioral Disorders in Mice by Mediating Gut-Brain-Axis Balance.

Ulcerative colitis (UC) is associated with brain neurotransmitter disorders and intestinal dysbiosis. Bacillus amyloliquefaciens fmb50 produces the lipopeptide surfactin, which has a wide range of biological activities. However, the effects of surfactin on DSS-induced colitis have not been reported. In the present study, oral surfactin significantly ameliorated colitis in a mouse model and reduced depression-like behavior, such as slowed walking speed, shortened movement distance in the open field test, and weakened exploration ability in the light-dark shuttle test. Surfactin noticeably improved gut microbial dysbiosis, intestinal barrier dysfunction in the colon, and blood-brain barrier dysfunction in the brain. Furthermore, the colon levels of occludin were upregulated by 68.51%, and the brain levels of occludin and ZO-1 were upregulated by 77.81% and 36.42%, respectively. Surfactin supplementation also inhibited inflammatory responses by inactivating the tumor necrosis factor-α (TNF-α), nuclear factor kappa-B (NF-κB), and NLRP3 signaling pathways in the colon and brain. Thus, we believe that surfactin improved the behavioral disorders by upregulating the levels of 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), norepinephrine (NE), and brain-derived neurotrophic factor (BDNF), suppressing the inflammatory responses, and improving the blood-brain barrier dysfunction. Surfactin also reduced the abundances of gut microbes that are related to colitis, especially targeting facultative anaerobes of the phylum Proteobacteria, and it increased the abundance of beneficial bacteria such as Lactobacillus and unidentified Prevotella. Combined with its nontoxic nature observed in this long-term study in mice, oral surfactin might be a promising intervention strategy for preventing colitis by acting on the microbiota-gut-brain axis.

Maltose-Enhanced Exopolysaccharide Synthesis of Lactiplantibacillus plantarum through CRP-like Protein.

Carbon sources alter the synthesis of exopolysaccharides (EPS) in Lactiplantibacillus plantarum. Maltose increased the EPS production of L. plantarum 163 6.5-fold. Subsequently, EPS production, transcriptome, and proteome were analyzed using glucose or maltose to further clarify the regulatory mechanism. A cAMP receptor protein (UniProtKB: F9UNI5) has been identified to control EPS synthesis in the presence of cAMP by binding to the EPS synthesis promoter Pcps4A-J. Overexpression of the cAMP synthesis gene cyaA increased cAMP content and EPS production 4.5- and 2.2-fold, respectively. Furthermore, yogurt produced with L. plantarum 163-cyaA had a similar viscosity to that of commercial Greek yogurt; it had 20 and 83.7% greater viscosity than that produced with L. plantarum 163 with maltose and glucose, respectively. These findings indicated that L. plantarum 163-cyaA has potential applications in the production of functional fermented dairy products.

Probiotic Yogurt Alleviates High-Fat Diet-Induced Lipid Accumulation and Insulin Resistance in Mice via the Adiponectin Pathway.

A high-fat diet (HFD) easily contributes to the pathogenesis of obesity and insulin resistance. Obesity and insulin resistance have been clinical and public health challenges all over the world. Probiotic-fermented yogurt is one type of popular and functional beverage in people's daily lives. This study mainly explored the lipid- and glucose-lowering effects of Lactobacillus acidophilus NX2-6-fermented yogurt (LA-Y) in HFD-fed mice. The results showed that LA-Y administration improved the lipid profile in the serum and liver, reduced fasting blood glucose levels, and enhanced insulin sensitivity. Protein analysis showed that LA-Y treatment promoted fatty acid oxidation and suppressed de novo lipogenesis in the adipose tissue and liver. LA-Y effectively alleviated glucose metabolism disorders by activating the insulin signaling pathway, suppressing gluconeogenesis in the liver and muscle, reducing the concentration of pro-inflammatory cytokines in the serum, and promoting glycolysis and gluconeogenesis in the small intestine. LA-Y supplementation also promoted fat browning via the adiponectin/AMPKα/PGC-1α/UCP1 pathway and enhanced mitochondrial biogenesis in the liver and muscle by activating the adiponectin/AdipoR1/APPL1/AMPKα/PGC-1α pathway, leading to increased energy expenditure. Therefore, LA-Y may be a functional dairy food for preventing and alleviating diet-induced metabolic disorders.

LsrR-like protein responds to stress tolerance by regulating polysaccharide biosynthesis in Lactiplantibacillus plantarum.

In addition to their biological functions, polysaccharides assist Lactiplantibacillus plantarum in resisting harsh conditions. To enhance the polysaccharide biosynthesis and increase the survival of L. plantarum in gut environment. We analyzed the transcriptional regulators that regulated the polysaccharide biosynthesis. A new transcriptional inhibitor, LsrR (UniProtKB: Q88YH7), had been identified, which repressed polysaccharide synthesis by binding to the polysaccharide synthesis promoter cps4A-J (Pcps4A-J). The EPSs and CPSs production of L. plantarum 163 was reduced by 42 % and 36 % (p < 0.05), respectively, when lsrR was overexpressed. Furthermore, alkaline shock proteins Asp2 and Asp1, heat shock protein Hsp3, and an autoinducer-2 (AI-2) related quorum-sensing regulator Rrp6 recovered the synthesis of polysaccharides to 50, 33, 55, and 60 %, respectively, by inhibiting the LsrR activity. This suggested that LsrR regulates polysaccharide synthesis in response to external stress signals such as pH, temperature, and AI-2 concentration. Finally, we showed that polysaccharides increased the survival rate of L. plantarum (Lp163-ΔlsrR) by 2.1 times during lyophilization and enhanced its tolerance to pH 2.0 and 0.2 % bile salts by 15.3 and 60 times due to increased capsular thickness and enhanced the autoaggregation. We provide critical data regarding Lactobacillus survival during preservative lyophilization and under gastrointestinal conditions.

Promoted Spore Formation of Bacillus amyloliquefaciens fmbJ by its Secondary Metabolite Bacillomycin D Coordinated with Mn2.

In Bacillus, the spore formation process is associated with the synthesis and release of secondary metabolites. A large number of studies have been conducted to systematically elucidate the pathways and mechanisms of spore formation. However, there are no studies have explored the relationship between secondary metabolites and spores. In this study, we investigated the relationship between its secondary metabolite bacillomycin D (BD) and spores using the simpler dipicolonic acid fluorimetry assay for spore counting in Bacillus amyloliquefaciens fmbJ. Our results showed that BD could promote the spore formation of B. amyloliquefaciens fmbJ and had a synergistic effect with certain concentrations of Mn2+. When 15.6 mg/L of BD and 1 mM of Mn2+ were added, the number of fmbJ spores increased from 1.42 × 108 CFU/mL to 2.02 × 108 CFU/mL after 36 h of incubation. The expressions of spore formation (kinA, kinB, kinC, kinD, kinE and spo0A) and Mn-related genes (mntA, mntH, mneS, mneP) were studied by RT-PCR. The results indicated that BD and Mn2+ promoted the spore formation of fmbJ by stimulating the transcription of kinB, kinD and increasing the influence of spo0F-spo0A phosphorylation transmission. This study provided a new idea to improve the spore production of B. amyloliquefaciens and laid the foundation for its industrial production. Supplementary Information: The online version contains supplementary material available at 10.1007/s12088-022-01026-9.

Effect of Lactobacillus with Feruloyl Esterase-Producing Ability on Dextran Sodium Sulfate-Induced Ulcerative Colitis in Mice.

Ulcerative colitis (UC) is becoming an increasingly serious health problem. This study aimed to investigate the effect of a newly isolated Lactobacillus species that produces feruloyl esterase (FAEb) on dextran sodium sulfate (DSS)-induced UC in mice. In this study, FAEb supplementation slowed body weight loss and mitigated colon length shortening, the severity of fecal occult blood, and increases in the disease activity index (DAI) in UC model mice. FAEb supplementation was also shown to reduce the expression of proinflammatory factors, increase the antioxidant capacity, improve the production of beneficial short-chain fatty acids (SCFAs), upregulate the expression of tight junction proteins, reduce the histopathological scores, and reduce mucous barrier damage in the gut. Furthermore, FAEb supplementation was shown to inhibit inflammatory NF-κB signaling pathway activity, increase the abundance of beneficial bacteria, and regulate the balance of microbiota in the gut. These results suggest that FAEb may serve as a potential probiotic to prevent and treat UC.

The protective effects of sulforaphane on high-fat diet-induced metabolic associated fatty liver disease in mice via mediating the FXR/LXRα pathway.

Metabolic-associated fatty liver disease (MAFLD) is becoming the key factor in causing chronic liver disease all over the world. Sulforaphane (SFN) has been proven to be effective in alleviating many metabolic diseases, such as obesity and type 2 diabetes. In this study, C57BL/6 mice were fed a high-fat diet for 12 weeks to induce MAFLD and given SFN (10 mg per kg bw) daily. Our results showed that SFN not only improved the excessive accumulation of fat in the liver cells but also ameliorated liver and serum inflammatory and antioxidant levels. In addition, SFN can regulate bile-acid metabolism and fatty-acid synthesis by affecting their farnesoid X receptor (FXR)/liver X receptor alpha (LXRα) signaling pathway, ultimately alleviating MAFLD. Our study provides a theoretical basis for the mechanism by which SFN alleviates hepatic steatosis.

Surfactin Mitigates a High-Fat Diet and Streptozotocin-Induced Type 2 Diabetes through Improving Pancreatic Dysfunction and Inhibiting Inflammatory Response.

Surfactin from Bacillus amyloliquefaciens fmb50 was utilized to treat mice with type 2 diabetes (T2DM) induced by a high-fat diet/streptozotocin (HFD/STZ). Our group's earlier research indicated that surfactin could lower blood glucose and mitigate liver dysfunction to further improve HFD/STZ-induced T2DM through modulating intestinal microbiota. Thus, we further investigated the effects of surfactin on the pancreas and colon in mice with T2DM to elucidate the detailed mechanism. In the present study, mice with HFD/STZ-induced T2DM had their pancreatic and colon inflammation, oxidative stress, and endoplasmic reticulum stress (ERS) reduced when given oral surfactin at a dose of 80 mg/kg body weight. According to further research, surfactin also improved glucose metabolism by activating the phosphatidylinositol kinase (PI3K)/protein kinase B (Akt) signaling pathway, further protecting islets ß-cell, promoting insulin secretion, inhibiting glucagon release and mitigating pancreas dysfunction. Additionally, after surfactin treatment, the colon levels of the tight junction proteins Occludin and Claudin-1 of T2DM mice were considerably increased by 130.64% and by 36.40%, respectively. These findings revealed that surfactin not only ameliorated HFD/STZ-induced pancreas inflammation and dysfunction and preserved intestinal barrier dysfunction and gut microbiota homeostasis but also enhanced insulin sensitivity and glucose homeostasis in T2DM mice. Finally, in the further experiment, we were able to demonstrate that early surfactin intervention might delay the development of T2DM caused by HFD/STZ, according to critical biochemical parameters in serum.

Plantaricin A reverses resistance to ciprofloxacin of multidrug-resistant Staphylococcus aureus by inhibiting efflux pumps.

Overexpression of Staphylococcus aureus efflux pumps is commonly associated with antibiotic resistance, causing conventional antibiotics to be unsuccessful in combating multidrug-resistant bacterial infections. Reducing the activity of the efflux pump is an urgently required to tackle this problem. Here, we found that plantaricin A (PlnA), an antimicrobial peptide derived from Lactobacillus plantarum, had a synergistic effect with ciprofloxacin (CIP), reducing the IC90 of CIP by eight times. Subsequently, changes in membrane permeability, membrane potential, and reactive oxygen species (ROS) were determined; changes that did not explain the synergistic effect were previously observed. Ethidium bromide intake and efflux experiments showed that PlnA inhibited the function of the efflux pump by binding it and altering the structure of MepA, NorA, and LmrS. Then, a series of PlnA mutants were designed to explore the underlying mechanism; they showed that the charge and foaming of PlnA were the predominant factors affecting the structure of NorA. In a skin wound infection model, PlnA significantly reduced the dose of CIP, relieved inflammation, and promoted wound healing, indicating that PlnA and CIP synergy persisted in vivo. Overall, PlnA reduced the use of CIP for combination therapy, and allowing the continued used of CIP to kill MDR S. aureus. Multidrug-resistant Staphylococcus aureus threatens our life as a tenacious pathogen, which causes infections in hospitals, communities and animal husbandry. Various studies have showed that efflux pump inhibitors (EPIs) have been considered potential therapeutic agents for rejuvenating the activity of antibiotics. Unfortunately, small molecule EPIs exhibit several side effects that limit their use for clinical application. The present study showed a new EPI (plantaricin A) produced by Lactobacillus plantarum, which has low cytotoxicity and haemolysis and powerful inhibitory activity on efflux pumps. Therefore, it helps the design of new EPIs and controls the infection of MDR S. aureus.

Anti-toxicogenic fungi and toxin-reducing effects of bacillomycin D in combination with fungicides.

Mycotoxins are toxic secondary metabolites produced by fungus including Aspergillus and Fusarium. They can contaminate food and cause major health issues. Bacillomycin D (BD) is a natural antimicrobial lipopeptide generated by Bacillus that has excellent antifungal capabilities, but its high price prevents it from being widely used. Chemically produced and essential oil-based fungicides are also currently the most frequent types. In the study, the effects of combining BD with two types of fungicides on the growth of toxicogenic fungi as well as the generation of deoxynivalenol (DON) and fumonisin B1 (FB1) were examined. It was discovered that BD was more effective in suppressing molds than the other two types of fungicides, and it could be combined with synthetic or essential oil-based fungicides to provide a synergistic or additive effect. BD 31.25 µg/mL + Thymol (Thy) 7.81 µg/mL and BD 11.45 µg/mL + Cinnamon oil (Cin) 3.90 µg/mL inhibited F. graminearum, respectively. The combination of BD+Thy and BD+Cin at this concentration considerably reduced 60%-80% spore germination, when DON dropped below 300 ng/L. Furthermore, both combinations suppressed F. moniliforme growth and FB1 synthesis in a dose-dependent manner at lower concentrations. At an action dose of 2 MIC, FB1 production might be reduced to less than 100 ng/L. Our findings indicated that BD might interact synergistically with various fungicides, suggesting that it could be useful in the field of antifungal and toxicity reduction in food.

Lacticaseibacillus rhamnosus Fmb14 prevents purine induced hyperuricemia and alleviate renal fibrosis through gut-kidney axis.

Hyperuricemia is a critical threat to human health, and conventional medical treatment only aims to treat acute gouty arthritis. Purine diet-mediated chronic hyperuricemia and related syndromes are neglected in clinical therapeutics. In this study, the prevention ability of Lacticaseibacillus rhamnosus Fmb14, screened from Chinese yogurt, was evaluated in chronic purine-induced hyperuricemia (CPH) mice. After 12 weeks of Fmb14 administration, serum uric acid (SUA) in CPH mice decreased by 36.8 %, from 179.1 to 113.2 µmol/L, and the mortality rate decreased from 30 % to 10 %. The prevention role of Fmb14 in CPH was further investigated, and the reduction of uric acid by Fmb14 was attributed to the reduction of XOD (xanthine oxidase) in the liver and URAT1 in the kidney, as well the promotion of ABCG2 in the colon. Fmb14 administration Increased ZO-1 and Occludin expression in the colon and decreased fibrosis degree in the kidney indicated that Fmb14 administration had preventive effects through the gut-kidney axis in CPH. In specific, Fmb14 administration upregulated the diversity of gut microbiota, increased short-chain fatty acids (SCFA) by 35 % in colon materials and alleviated the inflammatory response by reducing biomarkers levels of IL-1ß, IL-18 and TNF-α at 11.6 %, 21.7 % and 26.5 % in serum, compared to CPH group, respectively. Additionally, 16 S rRNA sequencing showed 31.5 % upregulation of Prevotella, 20.5 % and 21.6 % downregulation of Ruminococcus and Suterella at the genus level, which may be a new gut microbial marker in hyperuricemia. In conclusion, Fmb14 ameliorated CPH through the gut-kidney axis, suggesting a new strategy to prevent hyperuricemia.