Archives of Microbiology最新文献

In this investigation, we systematically evaluated the immunomodulatory mechanisms of Methanobrevibacter smithii within the intestinal mucosal immune system using a murine oral gavage model. Flow cytometric analysis revealed that M. smithii administration significantly augmented TNF-α, IL-22, and IL-17 production in three key lymphocyte populations: group 3 innate lymphoid cells (ILC3s), CD4 + T cells, and CD8 + T cells. Notably, while the frequency of CD4 + T cells exhibited a reduction in the treatment cohort, CD8 + T cell proportions remained unchanged. Crucially, our comprehensive profiling demonstrated stable GM-CSF expression across all analyzed immune cell subsets. Although comparable activation patterns were observed in both ILC3s and T cell populations, multivariate analysis failed to identify linear correlations between their cytokine expression profiles. These findings demonstrate that Methanobrevibacter smithii actively modulates mucosal immunity through dual activation of innate (ILC3s) and adaptive (CD4+/CD8 + T cells) immune compartments, while highlighting the existence of non-redundant regulatory mechanisms within the intestinal immune ecosystem that merit further mechanistic exploration.

Campylobacter jejuni (CJ), a major cause of bacterial gastroenteritis, employs exosomes to disseminate virulence factors and disrupt host immune homeostasis. This study investigated the therapeutic potential of Arabic Gum (AZ) and Lactobacillus acidophilus (LA), individually and in combination, against CJ exosome-induced intestinal injury in rats, with emphasis on inflammasome-related signaling and microbiota modulation. Rats received AZ, LA, or both following CJ exosome exposure. Molecular analyses, histopathology, and microbiome sequencing were performed to elucidate mechanistic responses. CJ exosomes activated key virulence pathways and triggered pronounced inflammatory signaling characterized by alpha kinase 1 (ALPK1), Nuclear Factor Kappa B (NF-κB), and NOD-like Receptor Pyrin (NLRP) upregulation, accompanied by epithelial injury and dysbiosis. Treatment with AZ or LA alone attenuated inflammasome activation and partially restored immune and microbial balance. Notably, the combined treatment produced a synergistic effect, effectively suppressing ALPK1/NF-κB/NLRP signaling and reestablishing a more physiologic microbial community structure. These improvements were associated with reductions in pro-inflammatory cytokines and markers of tissue damage, as well as substantial recovery in intestinal, hepatic, and splenic architecture. Overall, AZ and LA significantly mitigated CJ exosome-mediated pathology, with the combined therapy demonstrating superior efficacy. The findings suggest that co-administration of AZ and LA may offer a promising dual-modal strategy to counteract CJ-induced inflammatory and microbial disturbances, potentially supporting future therapeutic approaches targeting exosome-mediated pathogenesis.

Plant growth-promoting rhizobacteria (PGPR) enhance plant growth, nutrient uptake and tolerance to biotic and abiotic stress through diverse microbial traits and plant-associated responses. At the molecular level, PGPR influences plant physiology by modulating phytohormone balance, nutrient signaling, and defense-related pathways. This review summarizes current knowledge on bacterial traits involved in nitrogen fixation, phytohormone production and modulation, siderophore-mediated iron acquisition and induced systemic resistance with an emphasis on molecular components and regulatory frameworks that have been experimentally characterized. Key signaling elements including reactive oxygen species, calcium fluxes, mitogen-activated protein kinase cascades, and hormone-responsive transcriptional regulators such as NPR1, are highlighted as central nodes in PGPR-associated plant responses. Where direct molecular causality remains unresolved, plant phenotypes observed are presented as evidence-based associations, and remaining knowledge gaps are identified. By integrating molecular components with functional outcomes, this review provides a conceptual framework for understanding how microbial traits interface with plant signaling networks and identifies priorities for future mechanistic research.

The mining and combustion of low-rank coal (LRC), in conjunction with the inadequate management of agricultural waste, notably cattle manure, constitutes a substantial environmental challenge, encompassing greenhouse gas (GHG) emissions and resource inefficiency. However, the co-utilization of these materials offers opportunities for sustainable waste valorization. This review identifies critical knowledge gaps and evaluates recent advances in the combination of LRC and manure for co-composting and bioresource recovery. The findings from the literature review suggest that microbial biodegradation and surfactant-assisted treatments can enhance the transformation of LRC into humic substances, whereas anaerobic digestion and composting can reduce methane emissions from manure. The co-composting of LRC and manure has been identified as a promising pathway to improve soil fertility and carbon sequestration, while mitigating GHG emissions. The present review aims to evaluate microbial, surfactant-assisted, and co-composting strategies for LRC and manure management, with emphasis on agricultural sustainability and climate mitigation. Nevertheless, challenges remain regarding process optimisation, scalability, and economic feasibility. The review concludes with a series of recommendations for future research aimed at integrating these biotechnologies into circular agricultural-energy systems.

Malassezia is a lipophilic yeast and a major commensal associated with the human skin and gut. It is responsible for several dermatological conditions and has been associated with human diseases, including certain cancers, yet the factors that trigger pathogenicity in this otherwise benign yeast remain poorly defined. Out of the 21 species of Malassezia that have been identified, 14 are associated with humans. In this study, we investigated how clinical strains of Malassezia furfur differ from the standard laboratory strain in terms of pathogenicity-associated elements and resistance features. In this study, we examined 58 pityriasis versicolor (PV) cases, presented with multiple hyperpigmented scaly macules over different parts of the body. From those infected lesions, skin scrapings were isolated and grown on lipid-rich media. We examined M. furfur strains isolated from PV patients and shortlisted six strains exhibiting pronounced pathogenic characteristics compared against the standard strain (MTCC1374/CBS1878). A comprehensive analysis was performed to assess growth kinetics, biofilm-forming capacity, lipase production, and tolerance to temperature, pH, and salinity. Our results indicate that the clinical variants of M. furfur reveal altered features, including increased biofilm formation, increased lipase production, and the ability to withstand several key parameters like pH, salinity, and temperature, which are indicative of their ability to withstand harsh environmental conditions. These characteristics represent clear signatures of increased pathogenic potential compared to the standard strain that collectively reflect an enhanced ability to withstand the fluctuating microenvironment of the human skin. The emergence of resistance-like features among clinical isolates may explain persistent colonisation and relapse frequently observed in PV and other Malassezia-associated disorders. This work highlights the importance of understanding how a common commensal yeast evolves virulence and resistance features, which may contribute to recurrent infections and confer therapeutic challenges.

The mucA gene is a major genetic determinant of mucoid conversion in Pseudomonas aeruginosa isolated from patients with cystic fibrosis (CF) and represents a frequent hotspot for adaptive mutations. Although the role of the mucA gene in pathogen adaptation and virulence has been progressively elucidated, a comprehensive and systematic synthesis of its emerging functions and regulatory networks remains lacking. Here, we summarize current advances in the study of mucA, including its evolutionary origin, structural and functional characteristics, regulatory role in alginate biosynthesis, its mutation-associated pathogenic effects, and emerging strategies to studying or targeting mucA-deficient strains. Overall, this review highlights mucA as an important component of stress response networks in P. aeruginosa and summarizes current evidence that may inform future studies on risk stratification in chronic infections.

The blood-brain barrier (BBB) plays a crucial role in protecting the central nervous system (CNS) from harmful substances but poses challenges to the effective delivery of many therapeutic drugs. While the inflammatory effects of lipopolysaccharides (LPS) are documented, the combined effects of specific LPS types on BBB integrity require further investigation. This study investigates the distinct and combined impacts of LPS derived from Escherichia coli (EC) and Bacteroides fragilis (BF) on BBB integrity. A range of assays was employed, including Limulus amebocyte lysate (LAL) endotoxin detection, CCK-8 cell viability assays, transepithelial electrical resistance (TEER) measurement, FITC-Dextran permeability, immunofluorescence and Western blot analysis of NF-κB p65 and phosphorylated p65 (p-p65) nuclear translocation, tight junctions (TJs) proteins (ZO-1, claudin-5, occludin), inflammation cytokines (TNF-α, IL-6) and COX-2 levels by qPCR and ELISA, Rhodamine 123 (Rh123) efflux assays, and Evans Blue (EB) staining in mice to assess BBB permeability in vivo. The results showed that EC-LPS had higher endotoxin activity compared to BF-LPS (EU ratio of 4.7:1), and despite equal EU concentrations, EC-LPS induced a stronger inflammatory response and more significant BBB disruption. Notably, the co-treatment group (EC-LPS + BF-LPS) showed no synergistic effect on BBB permeability, with BF-LPS antagonizing the effect of EC-LPS. Further confirmation through TLR4 and NF-κB inhibitors revealed that this BBB permeability mechanism is TLR4 receptor and NF-κB pathway-dependent.