ArticlemBio2015
Toxin synthesis by Clostridium difficile is regulated through quorum signaling.
Article in mBio, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
69 citing papers in PubMed, 116 citations in OpenAlex.
- Metabolic plasticity enables Clostridioides difficile growth in coculture with neutrophils and other mammalian cells.Anaerobe · 2025Article
- In-depth characterization of accessory gene regulator loci and associated virulence factors inCurrent research in microbial sciences · 2025Article
- Article
- Causal role of the gut microbiome in certain human diseases: a narrative review.eGastroenterology · 2024Review
- Overcoming donor variability and risks associated with fecal microbiota transplants through bacteriophage-mediated treatments.Microbiome · 2024Article
- Defined microbial communities and their soluble products protect mice from Clostridioides difficile infection.Communications biology · 2024Article
- Antibiotics and antibiotic-associated diarrhea: a real-world disproportionality study of the FDA adverse event reporting system from 2004 to 2022.BMC pharmacology & toxicology · 2023Article
- Review of the Impact of Biofilm Formation on RecurrentMicroorganisms · 2023Review
- Bacillus velezensis DSM 33864 reduces Clostridioides difficile colonization without disturbing commensal gut microbiota composition.Scientific reports · 2023Article
- Biofilm Formation ofMicroorganisms · 2023Review
- Quorum-sensing, intra- and inter-species competition in the staphylococci.Microbiology (Reading, England) · 2023Review
- Chemical and biomolecular insights into theIsrael journal of chemistry · 2023Article
- Regulatory transcription factors ofCritical reviews in microbiology · 2023Review
- Low-toxinEmerging microbes & infections · 2022Article
- The quorum sensing peptide EntF* promotes colorectal cancer metastasis in mice: a new factor in the host-microbiome interaction.BMC biology · 2022Article
- Iron Effects onAntibiotics (Basel, Switzerland) · 2022Article
- Genetic and phenotypic characteristics of Clostridium (Clostridioides) difficile from canine, bovine, and pediatric populations.Anaerobe · 2022Article
- Mechanisms and Applications of Bacterial Sporulation and Germination in the Intestine.International journal of molecular sciences · 2022Review
- Autoinducing peptide-based quorum signaling systems in Clostridioides difficile.Current opinion in microbiology · 2022Review
- Regulation of Clostridioides difficile toxin production.Current opinion in microbiology · 2022Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledClostridium difficile infection (CDI) is dramatically increasing as a cause of antibiotic- and hospital-associated diarrhea worldwide. C. difficile, a multidrug-resistant pathogen, flourishes in the colon after the gut microbiota has been altered by antibiotic therapy. Consequently, it produces toxins A and B that directly cause disease. Despite the enormous public health problem posed by this pathogen, the molecular mechanisms that regulate production of the toxins, which are directly responsible for disease, remained largely unknown until now. Here, we show that C. difficile toxin synthesis is regulated by an accessory gene regulator quorum-signaling system, which is mediated through a small (<1,000-Da) thiolactone that can be detected directly in stools of CDI patients. These findings provide direct evidence of the mechanism of regulation of C. difficile toxin synthesis and offer exciting new avenues both for rapid detection of C. difficile infection and development of quorum-signaling-based non-antibiotic therapies to combat this life-threatening emerging pathogen. IMPORTANCE: Clostridium difficile infection (CDI) is the most common definable cause of hospital-acquired and antibiotic-associated diarrhea in the United States, with the total cost of treatment estimated between 1 and 4.8 billion U.S. dollars annually. C. difficile, a Gram-positive, spore-forming anaerobe, flourishes in the colon after the gut microbiota has been altered by antibiotic therapy. As a result, there is an urgent need for non-antibiotic CDI treatments that preserve the colonic microbiota. C. difficile produces toxins A and B, which are directly responsible for disease. Here, we report that C. difficile regulates its toxin synthesis by quorum signaling, in which a novel signaling peptide activates transcription of the disease-causing toxin genes. This finding provides new therapeutic targets to be harnessed for novel nonantibiotic therapy for C. difficile infections.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.