Divine Aleru, Microbiome Medicine Research Coordinator

This study defines how the NetB toxin from Clostridium perfringens forms membrane pores and drives enteric disease, linking toxin structure to microbiome-associated virulence and epithelial damage.

This review explains how Clostridium perfringens causes necrotic disease through microbiome disruption, toxin production, and immune suppression. Microbiome imbalance increases pathogen abundance, while microbial metabolites can reduce virulence, highlighting microbiome stability as a key protective factor and therapeutic target in necrotic enteritis and systemic infection.

This genome sequencing study revealed how Clostridium perfringens survives in the gut microbiome and causes disease. Virulence genes, toxin regulation, and host-dependent metabolism enable tissue destruction and rapid growth, highlighting microbiome-driven pathogenicity and identifying genetic targets for improved diagnostics and therapeutic interventions.

This genomic study identified a Clostridium perfringens strain carrying both enterotoxin and NetB toxin genes, revealing microbiome-driven virulence evolution through plasmid transfer. The findings highlight microbiome gene exchange as a key driver of pathogenicity and emphasize the need for genomic surveillance to detect emerging toxin-producing strains.

This genomic study of 372 Clostridium perfringens strains revealed extreme genetic diversity, widespread toxin genes, and high antimicrobial resistance. Microbiome-associated virulence factors enable host colonization, intestinal disease, and zoonotic transmission, highlighting the importance of microbiome surveillance and genomic diagnostics to prevent foodborne illness and antibiotic-resistant infections.

This review explains how Clostridium perfringens shifts from a gut microbiome commensal to a toxin-producing pathogen. Genomic diversity, toxin genes, antibiotic resistance, and microbiome disruption drive gastrointestinal disease, including food poisoning and necrotizing enterocolitis, highlighting its importance as a microbiome biomarker and therapeutic target.

This review explains how Clostridium perfringens functions as a gut microbiome commensal and toxin-producing pathogen. Toxin genes, plasmid virulence, antimicrobial resistance, and microbiome disruption drive gastrointestinal disease, antibiotic-associated diarrhea, and food poisoning, highlighting the importance of toxin detection and microbiome stability in clinical management.

Fusobacterium nucleatum is a Gram-negative, anaerobic bacterium commonly found in the oral cavity, where it plays a crucial role in the formation of biofilms. Beyond its presence in the mouth, Fn is implicated in a variety of systemic conditions, including periodontal disease, colorectal cancer, and inflammatory bowel disease. Known for its ability to coaggregate with other bacteria, Fn’s pathogenic potential is magnified in dysbiotic microbial communities, making it a key player in polymicrobial infections. The bacterium utilizes multiple virulence factors such as FadA and Fap2, which facilitate adhesion to host tissues and immune evasion, ultimately contributing to its role in chronic and inflammatory diseases.

This study reveals that Fusobacterium animalis is linked to increased immune gene expression and microsatellite instability in CRC. It suggests Fusobacterium’s role in tumor progression, offering insights into potential biomarkers and therapeutic strategies for CRC patients.

This study uncovers the dual role of HmuF and FldH in Fusobacterium nucleatum’s anaerobic heme degradation, highlighting their functions in heme trafficking and reduction of anaerobilin, with implications for targeted therapeutic strategies.

This study explored the role of Fusobacterium nucleatum’s outer membrane proteins, Fap2 and RadD, in inducing cell death in human lymphocytes. It focused on how these proteins, identified as part of the type Va autotransporter family, contribute to the bacterium’s virulence. The study examined the mechanisms by which Fap2 and RadD trigger […]

This study reveals Fn-Dps, a virulence factor from Fusobacterium nucleatum, as a key player in colorectal cancer metastasis, immune evasion, and erythrocyte disruption, highlighting its potential as a target for therapeutic intervention and a biomarker for CRC.

This review explores the role of Fusobacterium nucleatum in colorectal cancer, its impact on tumor progression, metastasis, immune modulation, and chemoresistance, and proposes potential strategies for CRC prevention and treatment.

This study identifies Fusobacterium nucleatum W1481 as a potential new subspecies, with unique genomic islands and antibiotic resistance mechanisms, highlighting its role in periodontal disease and potential for further clinical research.

This study explores how Fusobacterium nucleatum promotes chemoresistance in colorectal cancer by activating autophagy and altering microRNA expression, highlighting potential therapeutic avenues.

This study identifies Fusobacterium nucleatum as a significant pathogen in primary endodontic infections, strongly associated with clinical features like pain and swelling. The higher detection rate by PCR emphasizes the need for targeted treatments to eliminate this bacterium and improve endodontic outcomes.

This study investigated the impact of Fusobacterium nucleatum’s FadA antigen on the competing endogenous RNA (ceRNA) network involving ANXA2 (Annexin A2) and its role in the progression of colorectal cancer (CRC) and adenomatous polyps (AP). Specifically, it examined how the FadA antigen contributes to the upregulation of ANXA2 through interactions with LINC00460 […]

This study shows that Fusobacterium nucleatum-derived extracellular vesicles activate the AIM2 inflammasome in intestinal epithelial cells, leading to pyroptosis and exacerbating ulcerative colitis. Targeting this pathway may offer a promising therapeutic strategy to alleviate UC progression.

This study explores how Fusobacterium nucleatum contributes to chemoresistance in colorectal cancer by activating the autophagy pathway through the downregulation of specific microRNAs, offering potential targets for improving chemotherapy outcomes.

This study identifies MegL as the major enzyme for H2S production in Fusobacterium nucleatum, crucial for bacterial fitness, antibiotic resistance, and virulence in preterm birth, offering potential therapeutic targets to manage F. nucleatum infections.

This study reveals a significant increase in penicillin-resistant Fusobacterium nucleatum in children due to beta-lactamase production, highlighting the role of antimicrobial exposure in the rise of resistance and the need for alternative treatment strategies in pediatric infections.

This study investigated the production of beta-lactamase and antimicrobial susceptibility profiles of Fusobacterium nucleatum isolates from the oral microbiota of young children. The research aimed to identify the frequency of beta-lactamase production among different F. nucleatum subspecies, assess the associated resistance to antibiotics, and evaluate potential alternative treatments for infections caused by […]

This review discusses how Fusobacterium nucleatum adhesin RadD binds to CD147, promoting colorectal cancer proliferation. Targeting RadD may provide new therapeutic strategies for CRC treatment.

This study reveals that Fusobacterium nucleatum FadA promotes CRC through binding E-cadherin, activating beta-catenin signaling and inflammation. These findings suggest new diagnostic and therapeutic strategies targeting FadA to reduce CRC progression.