Probiotic products have attracted increasing attention for their potential to modulate the microbiota. However, most commercial products are designed for oral administration, and their probiotic properties relevant to topical use in the reproductive tract remain insufficiently evaluated. [Objective] To assess the probiotic properties of lactic acid bacteria (LAB) derived from probiotic products, with a particular focus on their potential for topical application, thus providing scientific evidence for their use in vaginal health. [Methods] Seven common oral probiotic products (P1-P7) containing at least two different LAB species were selected from major e-commerce platforms via keyword screening, along with one clinical probiotic product (P8). LAB strains were isolated and identified from these products. We evaluated the acid tolerance, as well as the growth characteristics under different pH conditions, of the isolates by culturing them in the media of varying pH values. The antimicrobial activities of the isolates were determined via co-culture assays with pathogenic microorganisms, while hemolysis assays and genomic comparison were conducted to assess safety. [Results] The isolation rates of LAB strains from P1 to P8 were 50.0% (2/4), 0 (0/4), 66.7% (2/3), 12.5% (1/8), 33.3% (2/6), 40.0% (2/5), 0 (0/7), and 100.0% (1/1), respectively. Most strains grew well at pH 6.0-7.0, and some maintained growth at pH 4.0. Strains P4 and P8 exhibited superior acid tolerance to the others. The inhibitory effects of different strains against common vaginal pathogens varied significantly. Strains P1-2, P5-1, P6-1 and P6-2 demonstrated moderate to strong broad-spectrum inhibitory activity against all tested pathogens. Other isolated strains except P8 exhibited inhibitory activity against Gardnerellavaginalis, while strain P8 showed weak inhibitory activities against the tested pathogens. Strains P4, P5-2, P6-1, and P6-2 achieved inhibition rates exceeding 99.73% against Candidaalbicans across all three tested inoculum concentrations, and strain P5-1 reached an inhibition rate of over 94.64%. None of the strains exhibited β-hemolytic activity, and no antibiotic resistance or virulence genes were detected. [Conclusion] Several LAB isolates from commercial probiotic products exhibited notable inhibitory activities against pathogenic microorganisms and demonstrated good safety profiles. Topical administration may therefore offer greater practical value in promoting female reproductive tract health.

[Objective] To evaluate the edible safety of Penicillium polonicum CK2023-1, a key strain responsible for flavor formation of traditional bacon in Chengkou, thus providing a scientific basis for developing microbial starter for bacon fermentation. [Methods] The genomic DNA sequence of P. polonicum CK2023-1 was determined via third-generation sequencing combined with second-generation sequencing and annotated via GO, KEGG, and antiSMASH databases. The spore suspension (1×10⁹ spores/kg) of CK2023-1was applied to cured meat surfaces, followed by 26 d local smoking in Chengkou. Non-volatile metabolites were analyzed via LC-MS/MS. Acute oral toxicity (7 d) and subacute oral toxicity (28 d) tests in mice were conducted to assess pathogenicity. [Results] The genome of CK2023-1 was 33.27 Mb, with the N₅₀ of 5 236 196 bp and the G+C content of 52.91%, containing 10 901 predicted coding genes (49.02% of the genome). Eighty-three biosynthetic gene clusters (BGCs) for secondary metabolites were identified, including known mycotoxin (verrucosidin) BGC. Compared with that in the toxigenic strain P. polonicum X6, the BGC in CK2023-1 exhibited an inversion. No mycotoxins were detected in fermented bacon, and neither acute nor subacute toxicity tests caused morbidity or mortality in mice. [Conclusion] P. polonicum CK2023-1 has a well-defined genomic structure, produces no mycotoxins, and is non-pathogenic, meeting the safety criteria for food-grade microbial strains.

To systematically analyze the current status and research trends and identify the key research hotspots in the field of gut microbiota and metabolic syndrome (MetS) from 2005 to 2024, thus providing references for future research and intervention strategies. Relevant literature on gut microbiota and MetS was retrieved and screened from the Web of Science Core Collection. Bibliometric tools such as VOSviewer, CiteSpace, and the R package bibliometrix were used to analyze the publication trends, countries and institutions, research themes, and emerging hotspots. A total of 4 210 relevant publications were included. The annual number of publications showed an increasing trend, which was particular rapid after 2010. China and the United States led in publication output, and major research findings were published in journals such as Nutrients, Gut, and Nature. Research hotspots primarily covered the fields of nutrition and diet, biochemistry and molecular biology, and microbiology. Keyword evolution analysis revealed a shift from early descriptive studies on gut microbiota composition to mechanism investigations focusing on dysbiosis-related pathways such as energy metabolism, inflammatory responses, and gut-organ axes. Co-occurrence analysis further indicated that key microbial metabolites (e.g., short-chain fatty acids and bile acids) and microbiota-targeted interventions (e.g., probiotics and fecal microbiota transplantation) had become focal points in recent studies. This bibliometric study comprehensively summarizes the research landscape of gut microbiota and MetS and highlights emerging trends and directions. Given the limitations of conventional therapies in terms of targeting specificity, patient adherence, and long-term safety, microbiota-based interventions offer a promising breakthrough for the prevention and treatment of MetS, providing valuable theoretical support for future precision medicine.

[Objective] By examining intracellular and extracellular metabolite changes in ectomycorrhizal fungi (ECMF) under acidic aluminum stress, we identified key resistance-related metabolites and pathways, aiming to elucidate the aluminum tolerance mechanisms from the perspective of metabolic physiology and offer a theoretical basis for using ECMF in restoring aluminum-contaminated forests. [Methods] Pisolithus tinctorius was cultured in vitro in the acidic medium (pH 3.8) containing 0.0 mmol/L or 1.0 mmol/L Al³⁺. Untargeted metabolomics was employed to analyze changes in intracellular and extracellular metabolite levels. [Results] Compared with that under the 0.0 mmol/L Al³⁺ treatment, the colony diameter of P. tinctorius under 1.0 mmol/L Al³⁺ stress decreased significantly by 23.67%. In addition, the intracellular levels of nucleotides including uridylic acid, cytidine monophosphate, uridine, uridine diphosphate, cytidine, and guanosine were upregulated under 1.0 mmol/L Al³⁺ stress. Extracellular levels of organic acids such as shikimic acid, fumaric acid, heptanoic acid, and tartaric acid, along with carbohydrates including l-arabinose, trehalose, sucrose, and glucose, were also upregulated. Pyrimidine metabolism and citric acid cycle pathways were enriched intracellularly, while ABC transporters and phosphotransferase system pathways were enriched extracellularly. The potential biomarkers identified in the intracellular environment was citric acid, and those identified in the extracellular environment were trehalose and tartaric acid. [Conclusion] Acidic aluminum stress inhibits the growth of P. tinctorius. Intracellularly, P. tinctorius maintains cellular homeostasis and energy supply through enhanced nucleotide accumulation and activation of the citric acid cycle. Extracellularly, P. tinctorius promotes organic acid secretion and carbohydrate efflux to resist aluminum toxicity and associated oxidative damage.

[Objective] To explore the influence of Acinetobacter pittii LSQ 3 on the biofilm formation of Bacillus velezensis LSQ 19 and analyze the genomic characteristics of strain LSQ 3. [Methods] The effect of the cell-free supernatant (CFS) of LSQ 3 on the biofilm formation of LSQ 19 was analyzed by crystal violet staining, cell surface property analysis, the phenol-sulfuric acid method, XTT reduction assay, and scanning electron microscopy (SEM). Whole-genome sequencing was employed to determine the taxonomic status of strain LSQ 3, and the biosynthetic gene clusters for secondary metabolites were predicted based on the whole-genome data. [Results] The CFS of strain LSQ 3 significantly inhibited the biofilm formation of strain LSQ 19, and the volume ratio of 10 µL bacterial suspension to 190 µL CFS was determined as the minimum inhibitory concentration (MIC). Compared with the control, the CFS of strain LSQ 3 at MIC significantly reduced the surface hydrophobicity, adhesion, extracellular polymeric substances (EPS) production rate, and biofilm metabolic activity, while significantly improving the self-aggregation ability of LSQ 19 cells. In the presence of the CFS at MIC, LSQ 19 failed to form a biofilm on the glass surface. Strain LSQ 3 was identified as A. pittii based on whole-genome sequencing data. Its genome size was 3 939 365 bp, with the G+C content of 38.82% and 3 601 DNA coding sequences. The genome contained multiple genes involved in biofilm formation and virulence factors. The antiSMASH analysis showed that the genome of strain LSQ 3 contained seven biosynthetic gene clusters for secondary metabolites. [Conclusion] The CFS of A. pittii LSQ 3 can inhibit the biofilm formation of B. velezensis LSQ 19. This study provides a theoretical basis and reference for the construction of synthetic bacterial communities from the perspective of biofilms.

Soil colloidal phosphorus (CP) is an active component that cannot be overlooked in the soil phosphorus cycle. Its occurrence forms and migration behavior significantly influence phosphorus bioavailability and environmental risks. This paper systematically reviews the multiscale regulatory mechanisms of microbial actions in CP transformation and migration. It focuses on chemical effects (e.g., proton secretion, iron reduction, and organic acid coordination), physical effects (e.g., extracellular polymer trapping and biofilm pore remodeling), and microbial community dynamics and molecular ecology three dimensions to elucidate how microbes drive CP activation, immobilization, and migration through interfacial reactions, functional gene expression, and community interactions. The paper further explores the synergistic effects of multiple factors on microbial regulation processes, including soil physicochemical properties, agricultural management practices, and emerging pollutants. It identifies current research gaps in cross-scale coupling, in situ characterization, and mechanism modeling, while providing theoretical foundations and research directions for enhancing soil phosphorus utilization and pollution control.

The gut structure and functional performance rely on the stable type and quantity of gut mucosal epithelial cells, whose stability depends on continuous proliferation, differentiation, and migration of intestinal stem cells (ISCs) located in the crypts. Interactions between gut microbiota and ISCs support the homeostasis of the gut ecosystem. Intestinal epithelial cells (IECs) differentiated from ISCs influence the composition and function of gut microbiota through secreting immunoglobulins, mucins, etc. Meanwhile, the microorganism-associated molecular patterns (such as lipoteichoic acid and lipopolysaccharides) and metabolites (such as short-chain fatty acids and bile acids) from gut microbiota form the unique gut microenvironment to regulate the activity of ISCs and the homeostasis of IECs. Regulating the activity of ISCs and gut health by modifying gut microbiota has become a focus of current research. Thus, this review elaborates on the impact of ISCs on the gut microbiota as well as the regulatory roles of gut microbiota and related metabolites on the proliferation and differentiation fate of ISCs, aiming to broaden the understanding of the interaction between gut microbiota and ISCs. It is expected to provide strategies and targets for the regulation on gut health.

[Objective] The type VI secretion system (T6SS) is a novel virulence factor of Edwardsiella tarda. E. tarda virulence protein P (EvpP) is an effector of the T6SS. To date, the functional mechanisms of EvpP are still poorly understood. This study aimed to comprehensively investigate the biological functions of EvpP and elucidate the roles of T6SS in the pathogenicity of E. tarda. [Methods] We constructed the evpP-deleted mutant (ΔevpP) and complemented strain (ΔevpP-C) to study the effects of evpP deletion on the biological characteristics of E. tarda and infection in macrophages. [Results] No significant differences were observed in the growth curves or physiological and biochemical properties among the wild-type (WT), ΔevpP, and ΔevpP-C. However, compared with WT, ΔevpP exhibited significantly reduced motility, biofilm formation, adhesion rate to RAW264.7 macrophages, intracellular proliferation capacity, and ability to induce host cell autophagy, while triggering increased secretion of tumor necrosis factor-α (TNF-α) by macrophages. The complementation of evpP-C did not fully restore the intracellular proliferation capability, but completely rescued the other phenotypic defects. [Conclusion] EvpP does not affect the growth or physiological and biochemical properties of E. tarda. However, it could enhance the bacterial motility, biofilm formation, adhesion to macrophages, intracellular proliferation, and autophagy, while suppressing TNF-α secretion in E. tarda-infected macrophages. These findings confirm that EvpP plays a critical role in the pathogenicity of E. tarda.

Antibiotic resistance (AR) in microorganisms has become a crucial challenge to global public health security. The acquirement of AR in microorganisms is often accompanied by a fitness cost. Typically, in an environment without antibiotics, the bacterial community with AR shows weaker competitiveness than susceptible bacteria, which makes antibiotic resistance genes (ARGs) a burden for bacteria. This article elaborates on the mechanisms underlying the generation of fitness costs and the corresponding measurement methods, provides examples to illustrate the fitness costs mediated by ARGs under different acquisition methods, and introduces the differences in fitness costs between chromosome-mediated and plasmid-mediated ARGs as well as their molecular mechanisms. Finally, it proposes prevention and control strategies for antibiotic resistant bacteria (ARB) based on fitness costs. This article reveals the biological law of the trade-off between antibiotic resistance and bacterial fitness and provides ideas for preventing and controlling the global public health security issues caused by ARB and ARGs.

[Objective] To investigate the regulatory effect of the cAMP receptor protein (CRP), a transcription factor in Acinetobacter baumannii, on the cas3 gene. [Methods] CRP was expressed and purified via a prokaryotic expression system. EMSA was employed to examine CRP binding to the cas3 promoter. qPCR was conducted to evaluate the regulatory effect of CRP on cas3 expression. To further confirm the regulatory function of CRP, we constructed a mutant strain Δcrp. The impact of crp deletion on A. baumannii virulence was then analyzed via the biofilm formation assay, adhesion and invasion assays with A549 cells, a Galleria mellonella model, and a murine model of bacterial infection. [Results] EMSA demonstrated that CRP specifically bound to the cas3 promoter. The qPCR results showed that cas3 transcription was downregulated (P<0.001) in Δcrp. Compared with the wild-type strain, Δcrp exhibited no significant difference in growth capacity but enhanced biofilm formation (P<0.001) as well as strengthened adhesion (P=0.003<0.050) and invasion (P<0.001) in A549 cells. Furthermore, Δcrp demonstrated a markedly increased lethality rate in G. mellonella within 72 h. Furthermore, the murine infection experiment revealed that Δcrp possessed higher colonization capacity in the lungs than the wild-type strain (P<0.001). [Conclusion] CRP acts as a transcriptional activator that directly binds to the cas3 promoter to activate its transcription, thereby attenuating the virulence and pathogenicity of A. baumannii.