Clostridium difficile and Clostridium perfringens research

This study shows that mouse-derived microbiota is more effective than human-derived microbiota in clearing C. difficile in a mouse model of recurrent infection.

This study identifies distinct growth and chaining properties in Clade 5 Clostridioides difficile strains using time-lapse microscopy, linked to the cmr switch sequence orientation.

This study identifies KipOTIA in C. difficile as a detoxifying enzyme that converts 5-oxoproline into a nutrient, supporting bacterial growth.

This study examines how intestinal proteases process C. perfringens enterotoxin (CPE) and shows that processed CPE retains cytotoxic activity.

The paper investigates the structural composition of Perfringolysin O (PFO) complexes, finding that they are predominantly hexameric and built from hexameric sub-complexes.

This study shows that cephalosporin resistance in C. difficile is due to inhibition of D,D-carboxypeptidases, not L,D-transpeptidases, and highlights the plasticity of PG biosynthesis.

This study profiles carbon metabolism in C. difficile clinical isolates, revealing lineage-specific metabolic capabilities and divergence in two emerging ribotypes.

This study compares the microbiome effects of ibezapolstat and other antibiotics in humanized mice, finding that ibezapolstat and fidaxomicin had smaller impacts on gut microbiome diversity than vancomycin and metronidazole.

This study identifies two glycosyltransferases involved in synthesizing glycolipids in C. difficile and highlights their role in bacterial physiology.

This paper evaluates a TcdB vaccine adjuvanted with a dual-TLR ligand liposome, showing complete protection against lethal CDI in mice and superior antibody and memory B cell responses compared to alum.

This study compares antimicrobial susceptibility testing of C. difficile across three media and three drugs, finding medium-dependent MIC differences and recommending FAA-HB for consistency.

This study investigates the impact of a perR mutation on oxygen sensitivity, gene expression, and infection in C. difficile 630Δerm, finding no difference in infection outcomes but altered gene expression under ambient oxygen.

This study shows that C. difficile colonization in an in vitro model is not dependent on bile salts but relies on proline fermentation via Stickland pathway, with context-dependent effects.

The paper investigates why C. difficile colonization leads to varying disease outcomes by studying microbiota-humanized mice and identifying commensals that mitigate virulence.

This study shows how human gut microbiota interactions influence the long-term growth and evolutionary adaptations of C. difficile, including metabolic shifts and reduced disease severity.

This study shows that CDT toxin from Clostridioides difficile induces biofilm-like microcolonies, increasing colonization and persistence in intestinal models and infected mice.

This study uses MALDI-TOF MS and machine learning to classify C. difficile ribotypes, achieving high accuracy for some ribotypes but not all.

This study screens an antiviral library to identify novel compounds with potent anti-C. difficile activity, with some showing MICs comparable to vancomycin.

The paper models the structure and mechanism of the CPE-claudin-4 pore complex, revealing its hexameric architecture and cation selectivity.

This paper uses dual RNA-seq to study coding and non-coding RNA expression dynamics in C. difficile infection in mice, identifying new ncRNA genes and host miRNAs associated with infection.

This paper shows that an avirulent C. difficile strain, ST1-75, protects mice from virulent strain-induced colitis by outcompeting it through rapid amino acid depletion, suggesting potential as a biotherapeutic for CDI prevention.

The study shows that mice with the synthetic microbiota OMM19.1 are susceptible to C. difficile infection without antibiotics, with increased infection severity at higher doses.

This study presents cryo-EM structures of Clostridium perfringens enterotoxin bound to claudin-4, revealing its pore assembly mechanism and potential therapeutic strategies.

This study uses computational methods and metagenomic data to identify microbial strains that can inhibit CDI, supporting the design of live biotherapeutic products.

This study investigates how mutations in YabG affect C. difficile spore germination and substrate processing, showing altered substrate cleavage and expression patterns.

This study identifies gut microbiota interactions that inhibit C. difficile strains across nutrient environments, highlighting strain variability and nutrient context as key factors.

This study investigates glycogen metabolism's role in C. difficile virulence, finding that glycogen accumulation enhances spore resilience and disease relapse.

This study identifies a new family of LDTs in C. difficile that catalyze 3-3 peptidoglycan crosslinking, essential for viability and distinct from previously known YkuD domain LDTs.

This study shows that HtrA proteolytic activity affects its expression level and is necessary for C. difficile survival under acidic conditions.

The paper identifies a network of small RNAs that regulate sporulation in C. difficile by modulating translation of the master sporulation regulator Spo0A.