FEMS microbiology reviews最新文献

Staphylococcus aureus, a leading human pathogen, is increasingly recognized as a genotoxic bacterium that reshapes host cell integrity beyond its classical virulence traits. By inducing DNA damage in host cells, S. aureus activates host DNA damage response (DDR) pathways that can determine the balance between bacterial clearance and persistence. By promoting chromatin remodeling and epigenetic reprogramming, through bacterial effectors such as phenol-soluble modulins and infection-induced metabolic changes, S. aureus modulates host immune responses and supports intracellular persistence. These interconnected mechanisms link DNA damage with immune evasion, chronic inflammation, and long-term tissue remodeling, which may contribute to carcinogenesis in chronically infected tissues. Recognizing S. aureus as both an infectious and genotoxic agent opens new therapeutic perspectives. Targeting DDR and epigenetic pathways, or modulating trained immunity to restore protective responses, offers promising strategies to counteract bacterial persistence and limit infection-associated pathologies. This integrative perspective redefines the pathogenesis of S. aureus by linking its genotoxic activity to host cellular reprogramming, and underscores the potential of host-directed therapeutic strategies as complementary approaches to conventional antibiotic treatment. It establishes a conceptual framework for understanding S. aureus persistence and pathogenicity in the context of rising antibiotic resistance.

Clostridium scindens is a keystone bacterial species in the mammalian gut that, while low in abundance, has a significant impact on bile acid and steroid metabolism. Numerous studies indicate that the two most studied strains of C. scindens (i.e. ATCC 35704 and VPI 12708) are important for a myriad of physiological processes in the host. We focus on both historical and current microbiological and molecular biology work on the Hylemon-Björkhem pathway and the steroid-17,20-desmolase pathway that were first discovered in C. scindens. Our most recent analysis now calls into question whether strains currently defined as C. scindens represent two separate taxonomic groups. Future directions include developing genetic tools to further explore the physiological role of bile acid and steroid metabolism by strains of C. scindens and the causal role of these pathways in host physiology and disease.

Leprosy, caused by Mycobacterium leprae and Mycobacterium lepromatosis, remains a significant global health issue despite a tremendous decline in its worldwide prevalence in the last four decades. Mycobacterium leprae strains possess very limited genetic variability, making it difficult to distinguish them using traditional genotyping tools. Successful genome sequencing of a considerable number of M. leprae strains in the recent past has allowed development of improved genotyping tools for the molecular epidemiology of leprosy. Comparative genomics has identified distinct M. leprae genotypes and revealed their characteristic genomic markers. This review summarizes the progress made in M. leprae genomics, with special emphasis on the development of genotyping schemes. Further, an updated genotyping scheme is introduced that also includes the newly reported genotypes 1B_Bangladesh, 1D_Malagasy, 3K-0/3K-1, 3Q and 4N/O. Additionally, genotype-specific markers (single nucleotide polymorphisms, Insertion/Deletion) have been incorporated into the typing scheme for the first time to enable differentiation of closely related strains. This will be particularly useful for geographic regions where M. leprae strains characterized by a small number of genotypes are predominant. The detailed compilation of genomic markers will also enable accurate identification of M. leprae genotypes, using targeted analysis of variable regions. Such markers are good candidates for developing artificial intelligence-based algorithms for classifying M. leprae genomic datasets.

Iron and heme are crucial for pathogenic bacteria living in the human host but are not available in free form due to their binding by iron- and heme-sequestering proteins. Porphyromonas gingivalis causes dysbiosis in the oral microbiome and is considered a keystone pathogen in the onset and progression of periodontal diseases. Its ability to infect and multiply in host cells and its presence in distant tissues and fluids highlights its pathogenic versatility and explains the relationship between periodontal diseases and systemic or neurodegenerative diseases. Porphyromonas gingivalis has evolved specialized mechanisms that allow it to thrive in the host under adverse nutrient-limited conditions. This review presents the updated summary of the mechanisms of iron and heme acquisition by P. gingivalis, with a central role played by gingipains and the unique Hmu system. The potential role of other iron and heme acquisition systems, such as Hus and Iht, indicates the importance of the partially conserved heme biosynthesis pathway, involving homologs of the HemN, HemG, and HemH proteins. In light of increasing antibiotic resistance, difficulties with diagnosis, and drug administration, targeting the mechanisms of heme and iron acquisition of P. gingivalis represents a promising target for developing diagnostic tests, preventive or therapeutic strategies.

The coronavirus disease-19 pandemic has intensified interest in the global diversity of RNA viruses and their ability to jump hosts, with a notable expansion in the number of known betacoronaviruses in wild mammalian species, particularly bats. This has enabled vaccine development research to shift its focus to include a range of severe acute respiratory syndrome coronavirus-1 and severe acute respiratory syndrome coronavirus-2 related viruses from animal species, with the intention of developing broadly protective coronavirus vaccines and therapeutics. However, there is currently a lack of synthesis of this expanding knowledge base of viruses with potential to cause another severe disease outbreak. This has led to many vaccine trials considering protection against a small subset of known betacoronaviruses that poorly approximate the true diversity of this group of viruses. This review aims to synthesize information gained from the recent surge in betacoronavirus characterization, providing a catalogue of viruses exhibiting features that pose a risk to public health, together with a framework for assessing their likelihood of emergence and subsequent transmission through human populations. This information will help inform global pandemic preparedness measures before a novel betacoronavirus outbreak occurs.

Soil salinization, affecting 6.5% of arable land, deteriorates soil properties, reduces microbiota activity, hinders plant growth, and accelerates soil erosion. Excessive salt induces physiological drought and toxicity stress in plants, causing chlorosis, ion imbalances, and enzyme disruptions. This paper discusses microorganisms' resistance mechanisms, plant responses to salt stress, and summarizes current knowledge on bacterial osmoprotectants and their functions. It also reviews emerging agrobiotechnological strategies using microbial osmoprotectants to remediate salinized soils and enhance plant growth and productivity under salt stress. Osmoprotectants stabilize proteins, buffer redox potential, and retain water, thus alleviating osmotic stress and promoting bacteria and plants growth. Their application improves soil properties by enhancing aggregate formation, water permeability, moisture content, cation exchange capacity, and ion availability. Despite extensive literature on the function of osmoprotectants, the knowledge about their role in soil environments and agrobiotechnology applications remains limited. This paper indicates proposed research perspectives, including discovering new osmoprotectants, their correlation with soil fertilization, interactions with the soil microbiome, and plant responses. It also identifies significant knowledge gaps in these areas, highlighting the need for further studies to consolidate existing data and assess the potential of this approach to enhance soil health and crop productivity in saline environments.

Mpox in humans is a rash illness resulting from infection with monkeypox virus (MPXV). In 2022, a public health emergency of international concern (PHEIC) was declared with 115 countries reporting cases of Mpox. Most of these countries had not previously reported cases. This global outbreak was sustained primarily by human-to-human transmission within complex sexual networks. Whilst these cases were similar to previous clade II West African MPXV isolates, they were sufficiently genomically distinct to result in WHO recognizing two subclades within clade II: clade IIa and clade IIb. In 2024, a second PHEIC was declared, resulting from a marked increase in cases of clade I MPXV. In this scoping review, we compare the major clinical, epidemiological, and genomic features of the major mpox lineages and the implications for vaccination, transmission, infection control and treatment..

The disease burden from Legionella spp. infections has been increasing in many industrialized countries and, despite decades of scientific advances, ranks amongst the highest for waterborne diseases. We review here several key research areas from a multidisciplinary perspective and list critical research needs to address some of the challenges of Legionella spp. management in engineered environments. These include: (i) a consideration of Legionella species diversity and cooccurrence, beyond Legionella pneumophila only; (ii) an assessment of their environmental prevalence and clinical relevance, and how that may affect legislation, management, and intervention prioritization; (iii) a consideration of Legionella spp. sources, their definition and prioritization; (iv) the factors affecting Legionnaires' disease seasonality, how they link to sources, Legionella spp. proliferation and ecology, and how these may be affected by climate change; (v) the challenge of saving energy in buildings while controlling Legionella spp. with high water temperatures and chemical disinfection; and (vi) the ecological interactions of Legionella spp. with other microbes, and their potential as a biological control strategy. Ultimately, we call for increased interdisciplinary collaboration between multiple research domains, as well as transdisciplinary engagement and collaboration across government, industry, and science as the way toward controlling and reducing Legionella-derived infections.

The microbiomes of skin and gill mucosal surfaces are critical components in fish health and homeostasis by competitively excluding pathogens, secreting beneficial compounds, and priming the immune system. Disruption of these microbiomes can compromise their capacity for disease resilience and maintaining host homeostasis. However, the extent and nature of microbiome disruption required to impact fish health negatively remains poorly understood. This review examines how various stressors influence the community composition and functionality of fish skin and gill microbiomes, and the subsequent effects on fish health. Our findings highlight that the impact of stressors on skin and gill microbiomes may differ for different body sites and are highly context-dependent, influenced by a complex interplay of host-specific factors, stressor characteristics, and environmental conditions. By evaluating current knowledge on the genesis and homeostasis of these microbiomes, we highlight a strong influence of environmental factors especially on skin and gill microbiomes compared with fish gut microbiomes, which appear to be more closely regulated by the host's homeostatic and immunological systems. This review emphasizes the importance of understanding the ecology and plasticity of fish skin and gill microbiomes to identify critical thresholds for microbiome shifts that impact fish health and disease resilience.

Pathogenic microorganisms can infect a variety of niches in the human body. During infection, these microbes can only persist if they adapt adequately to the dynamic host environment and the stresses imposed by the immune system. While viruses entirely rely on host cells to replicate, bacteria and fungi use their pathogenicity mechanisms for the acquisition of essential nutrients that lie under host restriction. An inappropriate deployment of pathogenicity mechanisms will alert host defence mechanisms that aim to eradicate the pathogen. Thus, these adaptations require tight regulation to guarantee nutritional access without eliciting strong immune activation. To work efficiently, the immune system relies on a complex signalling network, involving a myriad of immune mediators, some of which are quite directly associated with imminent danger for the pathogen. To manipulate the host immune system, viruses have evolved cytokine receptors and viral cytokines. However, among bacteria and fungi, selected pathogens have evolved the capacity to use these inflammatory response-specific signals to regulate their pathogenicity. In this review, we explore how bacterial and fungal pathogens can sense the immune system and use adaptive pathogenicity strategies to evade and escape host defence to ensure their persistence in the host.