ArticleCellular and molecular life sciences : CMLS2017
Enteric glial cells are susceptible to Clostridium difficile toxin B.
Article in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 78 citations in OpenAlex.
- CSPG4 Mediates Inflammatory, Cell Death, and Senescence Responses in Enteric Glia Exposed to Clostridioides difficile Toxins.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Clostridioides difficile : A suspected pro-carcinogenic bacterium for gastrointestinal tumors.Chinese medical journal · 2026Review
- Xtr-mediated regulation of 4Fe-4S binding protein gene confers resistance to oxidative and antibiotic stress inFrontiers in microbiology · 2026Article
- Exploring the role of infectious pathogens in Alzheimer's disease neuroinflammation.Frontiers in cellular and infection microbiology · 2026Review
- Role of TLR4 in Enteric Glia Response to Clostridioides Difficile Toxins: Insights From In Vivo and In Vitro Studies.Journal of cellular and molecular medicine · 2025Article
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Clostridioides difficile meets the adenosine system: the art of manipulating host homeostasis.Journal of biomedical science · 2025Review
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- The sympathetic nervous system drives hyperinflammatory responses to Clostridioides difficile infection.Cell reports. Medicine · 2024Article
- PhosphoLipidome Alteration Induced byCells · 2024Article
- Exploring the Toxin-Mediated Mechanisms inMicroorganisms · 2024Review
- Special Issue "Bacterial Toxins and Cancer".International journal of molecular sciences · 2024Article
- Pro-Inflammatory Cytokines Enhanced In Vitro Cytotoxic Activity ofInternational journal of molecular sciences · 2024Article
- From diversity to disease: unravelling the role of enteric glial cells.Frontiers in immunology · 2024Review
- Review
- Review
- Cytotoxic synergism ofWorld journal of gastroenterology · 2023Review
- Neuroimmune regulation in Hirschsprung's disease associated enterocolitis.Frontiers in immunology · 2023Review
- Zinc restores functionality in porcine prepubertal Sertoli cells exposed to subtoxic cadmium concentrationFrontiers in endocrinology · 2023Article
- The Polyunsaturated Fatty Acid EPA, but Not DHA, Enhances Neurotrophic Factor Expression through Epigenetic Mechanisms and Protects against Parkinsonian Neuronal Cell Death.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile causes nosocomial/antibiotic-associated diarrhoea and pseudomembranous colitis. The major virulence factors are toxin A and toxin B (TcdB), which inactivate GTPases by monoglucosylation, leading to cytopathic (cytoskeleton alteration, cell rounding) and cytotoxic effects (cell-cycle arrest, apoptosis). C. difficile toxins breaching the intestinal epithelial barrier can act on underlying cells, enterocytes, colonocytes, and enteric neurons, as described in vitro and in vivo, but until now no data have been available on enteric glial cell (EGC) susceptibility. EGCs are crucial for regulating the enteric nervous system, gut homeostasis, the immune and inflammatory responses, and digestive and extradigestive diseases. Therefore, we evaluated the effects of C. difficile TcdB in EGCs. Rat-transformed EGCs were treated with TcdB at 0.1-10 ng/ml for 1.5-48 h, and several parameters were analysed. TcdB induces the following in EGCs: (1) early cell rounding with Rac1 glucosylation; (2) early G2/M cell-cycle arrest by cyclin B1/Cdc2 complex inactivation caused by p27 upregulation, the downregulation of cyclin B1 and Cdc2 phosphorylated at Thr161 and Tyr15; and (3) apoptosis by a caspase-dependent but mitochondria-independent pathway. Most importantly, the stimulation of EGCs with TNF-α plus IFN-γ before, concomitantly or after TcdB treatment strongly increased TcdB-induced apoptosis. Furthermore, EGCs that survived the cytotoxic effect of TcdB did not recover completely and showed not only persistent Rac1 glucosylation, cell-cycle arrest and low apoptosis but also increased production of glial cell-derived neurotrophic factor, suggesting self-rescuing mechanisms. In conclusion, the high susceptibility of EGCs to TcdB in vitro, the increased sensitivity to inflammatory cytokines related to apoptosis and the persistence of altered functions in surviving cells suggest an important in vivo role of EGCs in the pathogenesis of C. difficile infection.
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