Frontiers in Microbiology最新文献

Background: Helicobacter pylori (H. pylori) is a major gastric pathogen and class I carcinogen that causes chronic gastritis, peptic ulcer, and gastric cancer if left untreated. However, evidence on H. pylori prevalence and antimicrobial resistance in Kazakhstan, a country with a high gastric cancer burden, remains scarce. This study presents the first culture-based epidemiological investigation of H. pylori at a single center in Almaty.

Materials and methods: We conducted a cross-sectional study (2024-2025) of 150 dyspeptic patients in Almaty, Kazakhstan. A subset (n = 148) underwent rapid stool antigen (RAS) testing before gastric biopsy collection. Biopsy samples were cultured, and 86 (57.3%) yielded viable H. pylori isolates. Antimicrobial susceptibility testing by the agar dilution method was performed on these 86 isolates. Demographic and clinical data were analyzed, and a regional meta-analysis was conducted using data from recent studies across Central Asia and Russia to estimate pooled prevalence and clarithromycin resistance.

Results: Among 148 patients tested by RAS, 137 were positive. Resistance rates among 86 isolates were 87.2% to metronidazole, 33.7% to clarithromycin, and 3.5% to amoxicillin; no resistance was detected to minocycline or sitafloxacin. Multidrug resistance (defined as resistance to two or more antibiotics) was observed in 34.8% of isolates. The pooled H. pylori prevalence across Central Asian studies was 70% (95% CI: 59-80%), and pooled clarithromycin resistance was 29% (95% CI: 10-53%).

Conclusion: This study provides the first culture-based evidence of H. pylori infection and antimicrobial resistance in Kazakhstan. The high resistance to metronidazole and clarithromycin suggests a likely lower success of standard triple therapy in Almaty. Absence of resistance to minocycline and sitafloxacin supports their use in rescue regimens. These findings highlight the urgent need for national surveillance, updated treatment guidelines, and integration of molecular resistance monitoring to improve evidence-based management of H. pylori in Central Asia.

In the environment, Vibrio cholerae employs multiple strategies to resist predation by heterotrophic protozoa. For example, V. cholerae biofilms release toxic compounds, such as ammonium and pyomelanin, which can kill protists, such as Tetrahymena pyriformis. V. cholerae has also been shown to survive intracellularly and can escape as viable cells inside protozoan-expelled food vacuoles (EFVs). We previously reported that V. cholerae encased in EFVs are hyperinfectious, establishing an important link between anti-protozoal strategies and bacterial virulence. Although the intracellular resistance and escape of V. cholerae in EFVs have been reported, the molecular mechanisms behind this remain poorly understood. Here, we used single-cell transcriptomics of V. cholerae exposed to T. pyriformis and captured a total of 5,344 bacterial cells with heterogeneous gene expression. Cells with the same pattern of gene expression were grouped, resulting in 11 clusters of cells with a unique gene expression profile. Genes encoding outer membrane proteins, F₁F₀-Na⁺/H⁺ ATPase, metabolites, and toxins showed differential expression among the clusters. Furthermore, the motility-associated killing factor (Mak) toxins were differentially expressed. The V. cholerae mutants ΔmakA, ΔmakB, and ΔmakE were not capable of killing T. pyriformis, and ΔmakA and ΔmakE showed reduced survival inside EFVs compared to the wild type. These findings identify Mak toxins as key mediators of V. cholerae resistance to protozoan grazing and survival within EFVs. More broadly, our results provide mechanistic insight into grazing resistance, reveal factors facilitating persistence in EFVs, and underscore the interplay between environmental survival strategies and virulence in pathogenic bacteria.

To evaluate the biocontrol potential of the cell-free fermentation filtrate (CFFF) of Bacillus atrophaeus strain YL84 against Fusarium oxysporum f. sp. vasinfectum (FOV), this study systematically investigated the effects of the CFFF at various dilution ratios on FOV mycelial growth, conidial germination, cellular nucleic acid leakage, and malondialdehyde (MDA) content. Furthermore, the environmental stability of its antifungal activity was assessed. In addition, a dual-culture assay was conducted to evaluate the antagonistic activity of strain YL84 against FOV. The results of the dual-culture assay showed that strain YL84 significantly inhibited the growth of FOV, with an inhibition rate of 81.06%. Subsequently, the YL84 CFFF exerted significant inhibitory effects on FOV mycelial growth and conidial germination across different concentrations, achieving maximum inhibition rates of 75.68% and 77.56%, respectively. Notably, the treated mycelia exhibited a significant increase in cellular nucleic acid leakage and elevated levels of MDA, a product of lipid peroxidation, suggesting that the CFFF may disrupt the integrity of the pathogen's cell membrane. Stability assays revealed that the CFFF possessed substantial tolerance to high temperatures, ultraviolet irradiation, and hypersaline environments, although it remained sensitive to strongly alkaline conditions. Greenhouse pot experiments further confirmed the efficacy of YL84 CFFF in controlling cotton Fusarium wilt, with a maximum control efficacy of 69.21%. Moreover, the treatment induced the upregulation of defense-related enzyme activities in the plants, suggesting that the CFFF may function through both direct antifungal action and the elicitation of host-induced resistance. Component identification via Ultra-Performance Liquid Chromatography-Ion Mobility-Quadrupole Time-of-Flight Mass Spectrometry (UPLC-IMS-Q-TOF-MS) suggested that the filtrate is rich in structurally diverse compounds that were putatively identified as potential antimicrobial substances, predominantly classified as terpenoids and their derivatives. In conclusion, this study provides a systematic evaluation and supporting evidence for the further development of B. atrophaeus YL84 as a biocontrol agent.

Background: Mulberry leaf (Morus alba L.) is an edible plant that has been found to have medicinal effects in the treatment of hyperuricemia (HUA). The bioactive compounds of mulberry leaf and their mechanisms of action have not been determined yet.

Methods: In-silico methodologies were used to identify bioactive compounds and to determine the underlying mechanisms of mulberry leaf. In order to verify the biochemical mechanism and intestinal microbiota, in vivo experiments were conducted.

Results: Kaempferol was identified as the principal bioactive compound, while the key targets were AKT1 and TNF. Molecular docking and dynamics simulations revealed that AKT1-kaempferol and TNF-kaempferol complexes showed strong and stable binding pattern after a 100 ns simulation. In vivo studies demonstrated that kaempferol exerted significant anti-HUA effects. Specifically, kaempferol reduces AKT expression and phosphorylation, which may in turn reduces the oxidative stress and inflammatory pathways and signal transmission of the kidneys. Meanwhile, the application of kaempferol attenuated gut microbiota dysbiosis caused by HUA.

Conclusion: Kaempferol may regulate UA metabolism and inflammatory injury by modulating the AKT signaling pathway, and exert its effects on the gut-kidney axis and restoring gut microbiota composition.

Laguna Lake, the largest freshwater lake in the Philippines, has been reported to harbor antibiotic-resistant bacteria, posing health risks to the millions who depend on it. However, limited knowledge of antibiotic resistance genes (ARGs) in the lake highlights the need for a comprehensive assessment of its resistome. In line with this, we characterized ARGs in the West Bay of Laguna Lake using shotgun metagenomic sequencing based on six metagenomes collected from three stations across two sampling months at a single depth. ARGs were quantified from short reads, and assembled contigs containing these genes-antibiotic-resistant contigs (ARCs)-were analyzed to assess mobility through associations with plasmids and mobile genetic elements (MGEs). β-lactam resistance genes (0.023-0.048 copies per cell) were the most prevalent, corroborating previous reports. Meanwhile, the detection of bacitracin (0.013-0.028 cpc) and polymyxin (0.009-0.011 cpc) resistance genes raises new concerns, as resistance to these antibiotic classes has not been previously reported in the lake. Furthermore, 44.8 and 30.4% of ARCs were associated with plasmids and MGEs, respectively. ARCs carrying genes for resistance to β-lactams, chloramphenicol, and tetracyclines were frequently identified as mobile, indicating a high potential for horizontal gene transfer and suggesting possible antibiotic contamination in the lake. Overall, this study provides the first metagenomic insight into the resistome of Laguna Lake using short-read sequencing and highlights its role as an environmental reservoir of mobile ARGs. The findings underscore the need for expanded ARG surveillance to improve antimicrobial resistance risk prediction.

Introduction: To investigate the horizontal transmission of oral-gut microbiota in autism spectrum disorder (ASD) families and its potential implications for ASD pathogenesis.

Methods: The research employed a paired cohort design using family cohorts (23 ASD children/17 parents vs. 18 Non-ASD children/16 parents), conducting integrated microbiome and metabolomic analyses of oral and fecal samples.

Results: The findings revealed that ASD families exhibited significantly increased oral microbial species diversity alongside substantial alterations in gut microbiota composition, particularly demonstrating a lower Firmicutes/Bacteroidetes ratio (3.60/2.97) compared to Non-ASD families (5.59/5.35). Specific microbial changes included notable enrichment of Prevotella_9 in ASD gut microbiota. Metabolomic profiling identified significant disruptions in multiple metabolic pathways, including impaired L-rhamnose degradation and glutathione metabolism. The study observed coordinated oral-gut axis alterations through synchronized changes in Caulobacter and Serratia abundances, suggesting a distinct dysbiotic pattern along this microbial continuum. Additional metabolic findings demonstrated reduced levels of fecal glutamine and Ala-Gly in ASD children, with glycylproline exhibiting high predictive value for family typing (AUC = 0.91). Integrative analysis further revealed significant correlations between Holdemanella and various lipid metabolites.

Discussion: It indicates that ASD families display characteristic oral-gut microbiota interactions accompanied by metabolic abnormalities, potentially reflecting familial microbial transmission patterns that may contribute to ASD pathophysiology.

The mitogen-activated protein kinase (MAPK) pathway is a vital cellular signaling cascade that viruses exploit. When activated by viruses, this pathway also initiates the host's inflammatory response. This pathway has a crucial role in viral respiratory infections, serving as a key intersection where viral replication and host inflammation are coordinated. Some viruses activate this pathway to enhance their own replication while also triggering inflammatory responses in the host. Understanding this intersection is essential because therapeutic agents could target the same pathway to inhibit both viral replication and inflammation. This perspective considers targeting the MAPK pathway as a potential way to treat viral respiratory infections by suppressing viral replication and reducing inflammation.

This study evaluated the antimicrobial activity of pure juniper essential oil and its nanoemulsion formulations (2, 4, and 6%) against five foodborne and fish spoilage bacterial species, including Staphylococcus aureus, Salmonella Paratyphi A, Vibrio vulnificus, Photobacterium damselae and Proteus mirabilis. The GC-MS profile of pure juniper essential oil (EO) revealed thirty components, including α-pinene, which accounted for 90.05% of the total volatiles. The antimicrobial activity was studied by measuring the inhibition zone diameters by the agar well diffusion method and determining the minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) values by micro dilution method. A clear dose-response relationship was observed in nanoemulsion formulations; as EO concentration increased, inhibition zones enhanced and MIC/MBC values decreased. S. aureus showed inhibition even at 2%JNEO (~15 mm), reaching a maximum of 22.1 mm at 6%JNEO. Among Gram-negative pathogens, Vibrio vulnificus showed the highest susceptibility, particularly to pure juniper essential oil, as reflected by low MIC and MBC values. P. damselae and S. paratyphi A exhibited intermediate susceptibility (MIC 1.56-12.5 mg/mL; MBC 12.5-25 mg/mL), while P. mirabilis showed high resistance (MIC 12.5 mg/mL; MBC > 100 mg/mL) and only limited inhibition. Among the tested bacteria, Staphylococcus aureus and Vibrio vulnificus showed the highest susceptibility, with inhibition zones and MIC/MBC values decreasing in a concentration-dependent manner. This antimicrobial activity may be associated with the high α-pinene content of juniper essential oil. These results highlight the potential of juniper essential oil nanoemulsions as effective natural preservatives to control fish spoilage and foodborne bacteria in the seafood industry.

Introduction: Owing to its remarkable capacity to modify the aroma profile of wine, Lactiplantibacillus plantarum (L. plantarum) derived from wine has emerged as a potential starter for malolactic fermentation. However, the inadequate acid resistance of this bacterium severely restricts its application. In some bacterial species, GlnR is considered a universal transcriptional regulator in response to acid stress.

Methods: In this study, we determined the function of GlnR in the acid resistance of L. plantarum for the first time. RT-qPCR and yeast one-hybrid assays revealed a direct regulatory correlation between GlnR and genes associated with the glutamate metabolic pathway. Metabolomics analysis via liquid chromatography-mass spectrometry and fermentation studies confirmed that GlnR affected γ-aminobutyric acid (GABA) production.

Results: The growth and survival rate of the knockout strain XJ25-ΔglnR were significantly lower than those of the wild-type strain XJ25. GlnR can directly bind to the promotor regions of the genes glnA, gadB, and glms1, thereby upregulating gadB transcription while downregulating glnA and glms1 transcription, directing the increased metabolic flux toward GABA synthesis.

Discussion: We present evidence that GlnR plays a vital role in the glutamate metabolic pathway and is a positive transcriptional regulator that can control the acid resistance of L. plantarum XJ25. Although GlnR interacts with glnA, gadB, and glms1, additional studies are warranted to determine how this interaction affects its acid resistance.