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In this study, we (i) demonstrated how Fusobacterium nucleatum ( Fn ) infection triggers a complex interplay between oxidative stress and antioxidant defense mechanisms in endothelial cells, highlighting the critical role of the NOX4/NRF2 axis in driving endothelial senescence; (ii) revealed that early Fn infection activates NRF2, leading to transient antioxidant responses, but prolonged infection leads to NRF2 degradation, increasing oxidative stress and exacerbating endothelial dysfunction; and (iii) showed that targeting NOX4 or GSK3β restores redox balance, alleviates endothelial senescence, and improves vascular function. Our findings suggest that chronic oral infections, such as those caused by Fn , may contribute to vascular aging and the progression of atherosclerosis, underscoring the importance of oral health in preventing systemic cardiovascular diseases. This study provides new insights into the mechanisms of microbial-driven vascular aging and identifies potential therapeutic targets for combating age-related cardiovascular diseases.

Chlamydia trachomatis is a human pathogen and a prevalent agent of sexually transmitted diseases. The ability to survive and propagate within a protected intracellular niche leads directly to pathology indicative of Chlamydia -mediated disease. The reduced chlamydial genome leads to comparatively limited biosynthetic capacity, thereby necessitating parasitism of metabolites and other resources from the infected host cell. Chlamydia relies heavily on type III secreted effectors to interface with and co-opt host pathways to acquire resources. We demonstrate herein that the plasma membranes of infected cells represent a potential reservoir of resources required for optimal intracellular growth. Chlamydiae employ at least one type III secreted effector protein, translocated membrane-associated effector A (TmeA), to redirect material to the vacuole by manipulating Arp2/3-dependent actin polymerization. This pathway represents a distinct mechanism by which Chlamydia acquires resources and provides evidence for TmeA function during intracellular development.

National surveillance data show persistent racial and ethnic disparities in early childhood caries (ECC), but the underlying causes of these differences have not been determined. This study examined both functional and taxonomic differences in ECC-related microbial activity between two high-risk groups of children: African American (AA) and Latin American Hispanic (LAH). Metatranscriptomic profiling of paired non-caries and caries plaque revealed consistent population-level shifts in gene expression and enabled species-level attribution of metabolically active microbes in caries lesions. A core set of well-established cariogenic organisms was consistently present and highly over-expressed in caries of both groups, including , , , and . Beyond identifying the core organisms and functions active in lesions, we have also made two significant observations. First, the active communities in the two groups have substantially diverged: 4,900+ genes across 413 Kyoto Encyclopedia of Genes and Genomes Orthology (KO) groups were consistently (25%+ of samples) over-expressed in AA children, and 6,500+ genes across 382 KOs were consistently (57% of samples) over-expressed in LAH children. This reproducibility across multiple samples indicates robust group-level differences rather than random variation or single-sample effects. Second, although AA and LAH children exhibited similar functional responses to caries (sharing 1,392 KOs), these shifts were expressed by different bacterial species, indicating that distinct taxa may occupy similar metabolic niches in different groups. Taken together, these findings suggest that there is no single universal caries-associated microbiome; instead, a shared cariogenic core is necessary, but differences among the non-core taxa and their functional activity may be key to understanding ECC disparities. The disparity in tooth decay among young children has long been demonstrated in national surveillance data. While various factors including family, culture, access to health insurance, and medical infrastructure have been studied, the global transcriptomic perspective remains underexplored. Employing RNA-Seq technology, we examine functional and taxonomic differences in caries-associated microbial activity between two high-risk populations. Besides a core set of well-established cariogenic organisms, we observed significant and consistent differences in the active microbial communities between these two high-risk populations, African American (AA) and Latin American Hispanic (LAH) children. In AA children, and consistently showed the highest caries-related gene expression. In contrast, among LAH children, , sp., , , and were the primary drivers of gene expression in caries lesions. By identifying the unique microbial mechanisms and pathways active in each population, we can better define the core factors required for caries development and uncover how differences in microbial function contribute to persistent disparities.

Periodontitis is a common but complex oral disease that can lead to tooth loss and contribute to systemic health issues. Early and accurate diagnosis is essential for effective intervention, yet traditional diagnostic methods often rely on invasive clinical assessments that may miss early signs. This study demonstrates that salivary microbiome profiles can be used to classify both periodontal health and multiple periodontitis stages using a machine learning approach. By identifying the 20 key microbial taxa, including Actinomyces spp., we developed a non-invasive predictive model with high diagnostic accuracy. Importantly, the model was also able to detect early-stage disease and performed well across external data sets, highlighting its potential for broader clinical application. These findings suggest that a salivary microbiome-based diagnostic tool may support more precise, accessible, and early diagnosis of periodontitis in dental disease management.

Fusobacterium nucleatum is increasingly recognized as a pathobiont in mucosal diseases, including colorectal cancers and chronic airway infections, yet its functional interactions with co-colonizing microbiota remain poorly understood. Here, we demonstrate that F. nucleatum engages in bidirectional interactions with Segatella oris, a glycan-foraging anaerobe also enriched in mucin-rich environments. Through nutrient cross-feeding and transcriptional modulation, these interactions shape bacterial behavior and the host epithelial response. Notably, glycan degradation by S. oris enables F. nucleatum access to sialic acids, while F. nucleatum suppresses the expression of multiple polysaccharide utilization loci in S. oris, revealing a reciprocal ecological influence. Co-colonization of the airway epithelial surface also modulates gene expression linked to inflammation and cancer. These findings advance our understanding of polymicrobial dynamics at mucosal interfaces and highlight the importance of incorporating microbe-microbe-host interactions into reductionist models of infection and disease.

Bacteriophages, or phages, are viruses that can either kill or persist inside bacteria. Current interests in phage biology are in part ignited by the fact that they could be used to treat infections caused by antibiotic-resistant bacteria. However, most of our understanding of phage-bacterial interactions comes from in vitro models and/or in vivo gut models relying on altering the endogenous microbiota. Here, we report the finding of a novel phage, Eifel2, which specifically targets Citrobacter rodentium (CR), the mouse equivalent of human diarrheagenic E. coli pathogens. Despite effectively killing CR in vitro , CR and Eifel2 develop a co-existence relationship in mice with an intact microbiota. Although CR phage-resistant mutants emerge, host and microbial factors constrain their expansion. This work highlights the importance of studying phage therapy in host-pathogen contexts that include the complete microbiota, where therapeutic outcomes may rely on dynamic co-existence and containment rather than eradication.

Periodontal disease (PD) is a complex and infectious illness that begins with a disruption of bacterial homeostasis. This disease induces a host inflammatory response, leading to damage of the soft and connective tooth-supporting tissues. Moreover, in advanced cases, it can contribute to tooth loss. The aetiological factors of PDs have been widely researched, but the pathogenesis of PD has still not been totally clarified. There are a number of factors that have an effect on the aetiology and pathogenesis of PD. It is purported that microbiological, genetic susceptibility and lifestyle can determine the development and severity of the disease. The human body’s defence response to the accumulation of plaque and its enzymes is known to be a major factor for PD. The oral cavity is colonised by a characteristic and complex microbiota that grows as diverse biofilms on all mucosal and dental surfaces. The aim of this review was to provide the latest updates in the literature regarding still-existing problems with PD and to highlight the role of the oral microbiome in periodontal health and disease. Better awareness and knowledge of the causes of dysbiosis, environmental risk factors and periodontal therapy can reduce the growing worldwide prevalence of PDs. The promotion of good oral hygiene, limiting smoking, alcohol consumption and exposure to stress and comprehensive treatment to decrease the pathogenicity of oral biofilm can help reduce PD as well as other diseases. Evidence linking disorders of the oral microbiome to various systemic diseases has increased the understanding of the importance of the oral microbiome in regulating many processes in the human body and, thus, its impact on the development of many diseases.

Medicinal plants are rich sources of valuable molecules with various profitable biological effects, including antimicrobial activity. The advantages of herbal products are their effectiveness, relative safety based on research or extended traditional use, and accessibility without prescription. Extensive and irrational usage of antibiotics since their discovery in 1928 has led to the increasing expiration of their effectiveness due to antibacterial resistance. Now, medical research is facing a big and challenging mission to find effective and safe antimicrobial therapies to replace inactive drugs. Over the years, one of the research fields that remained the most available is the area of natural products: medicinal plants and their metabolites, which could serve as active substances to fight against microbes or be considered as models in drug design. This review presents selected flavonoids (such as apigenin, quercetin, kaempferol, kurarinone, and morin) and tannins (including oligomeric proanthocyanidins, gallotannins, ellagitannins, catechins, and epigallocatechin gallate), but also medicinal plants rich in these compounds as potential therapeutic agents in oral infectious diseases based on traditional usages such as Agrimonia eupatoria L., Hamamelis virginiana L., Matricaria chamomilla L., Vaccinium myrtillus L., Quercus robur L., Rosa gallica L., Rubus idaeus L., or Potentilla erecta (L.). Some of the presented compounds and extracts are already successfully used to maintain oral health, as the main or additive ingredient of toothpastes or mouthwashes. Others are promising for further research or future applications.

There is a growing level of interest in the potential role inflammation has on the initiation and progression of malignancy. Notable examples include Helicobacter pylori -mediated inflammation in gastric cancer and more recently Fusobacterium nucleatum -mediated inflammation in colorectal cancer. Fusobacterium nucleatum is a Gram-negative anaerobic bacterium that was first isolated from the oral cavity and identified as a periodontal pathogen. Biofilms on oral squamous cell carcinomas are enriched with anaerobic periodontal pathogens, including F. nucleatum, which has prompted hypotheses that this bacterium could contribute to oral cancer development. Recent studies have demonstrated that F. nucleatum can promote cancer by several mechanisms; activation of cell proliferation, promotion of cellular invasion, induction of chronic inflammation and immune evasion. This review provides an update on the association between F. nucleatum and oral carcinogenesis, and provides insights into the possible mechanisms underlying it.

Mounting evidence suggests a causal relationship between specific bacterial infections or microbial compositions and the development of certain malignant neoplasms. In this study, we performed research through 16S rRNA amplicon sequencing, qPCR and fluorescence in situ hybridization to certify the relationship between periodontal pathogens and oral squamous cell carcinoma (OSCC). Subgingival plaque, cancer and paracancerous tissues from 6 patients with OSCC were selected for mapping bacterial profiles by 16S rRNA amplicon sequencing. The research showed that periodontal pathogens were enriched in cancer and paracancerous tissues, while the bacterial profiles were similar between the cancer tissues and subgingival plaque. Furthermore, the relative abundance of Porphyromonas gingivalis , Fusobacterium nucleatum and Streptococcus sanguinis was detected in 61 cancer tissues, paracancerous tissues and subgingival plaque samples and in 30 normal tissues by qPCR. The results revealed that P. gingivalis and F. nucleatum existed at higher levels in cancer tissue than in normal tissues and were correlated with subgingival plaques. P. gingivalis was detected using a special oligonucleotide probe in 60.7% of OSCC tissues, 32.8% of paracancerous tissues and 13.3% of normal tissues. Relevance analysis showed that P. gingivalis infection was positively associated with late clinical staging, low differentiation and lymph node metastasis in patients with OSCC, which was accompanied by deeper periodontal pockets, severe clinical attachment loss and loss of teeth. This study revealed that there might be a close relationship between oral microorganisms, particularly periodontal pathogens, and OSCC, which might enrich the pathogenesis of oral squamous carcinoma.