ArticleScientific reports2017
Enteric glial cells counteract Clostridium difficile Toxin B through a NADPH oxidase/ROS/JNK/caspase-3 axis, without involving mitochondrial pathways.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 30 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
- Short-chain fatty acids mitigate inflammation and associated metabolic programming of human stem cell-derived enteric glial cells.Journal of neuroinflammation · 2026Article
- Article
- In Vitro Manipulation of Gene Expression in Enteric Glial Cells.Methods in molecular biology (Clifton, N.J.) · 2026Article
- The role of the enteric nervous system in the pathogenesis of Clostridioides difficile infection.Nature reviews. Gastroenterology & hepatology · 2025Review
- Mechanisms ofFrontiers in cellular and infection microbiology · 2025Review
- From diversity to disease: unravelling the role of enteric glial cells.Frontiers in immunology · 2024Review
- Review
- Review
- Cytotoxic synergism ofWorld journal of gastroenterology · 2023Review
- Adenosine receptors differentially mediate enteric glial cell death induced byFrontiers in immunology · 2022Article
- Role of Pannexin-1-P2X7R signaling on cell death and pro-inflammatory mediator expression induced byFrontiers in immunology · 2022Article
- S100B Inhibition Attenuates Intestinal Damage and Diarrhea Severity DuringFrontiers in cellular and infection microbiology · 2021Article
- Host Immune Responses toFrontiers in microbiology · 2021Review
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- Invisible steps for a global endemy: molecular strategies adopted byTherapeutic advances in gastroenterology · 2021Review
- Proinflammatory Cytokines: Possible Accomplices for the Systemic Effects ofJournal of inflammation research · 2021Article
- Crosstalk between Long-Term Sublethal Oxidative Stress and Detrimental Inflammation as Potential Drivers for Age-Related Retinal Degeneration.Antioxidants (Basel, Switzerland) · 2020Article
- Article
- Shenshuaikang Enema, a Chinese Herbal Remedy, Inhibited Hypoxia and Reoxygenation-Induced Apoptosis in Renal Tubular Epithelial Cells by Inhibiting Oxidative Damage-Dependent JNK/Caspase-3 Signaling Pathways Using Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enteric glial cells (EGCs) are components of the intestinal epithelial barrier essential for regulating the enteric nervous system. Clostridium difficile is the most common cause of antibiotic-associated colitis, toxin B (TcdB) being the major virulence factor, due to its ability to breach the intestinal epithelial barrier and to act on other cell types. Here we investigated TcdB effects on EGCs and the activated molecular mechanisms. Already at 2 hours, TcdB triggered ROS formation originating from NADPH-oxidase, as demonstrated by their reduction in the presence of the NADPH-oxidase inhibitor ML171. Although EGCs mitochondria support almost completely the cellular ATP need, TcdB exerted weak effects on EGCs in terms of ATP and mitochondrial functionality, mitochondrial ROS production occurring as a late event. ROS activated the JNK signalling and overexpression of the proapoptotic Bim not followed by cytochrome c or AIF release to activate the downstream apoptotic cascade. EGCs underwent DNA fragmentation through activation of the ROS/JNK/caspase-3 axis, evidenced by the ability of ML171, N-acetylcysteine, and the JNK inhibitor SP600125 to inhibit caspase-3 or to contrast apoptosis. Therefore, TcdB aggressiveness towards EGCs is mainly restricted to the cytosolic compartment, which represents a peculiar feature, since TcdB primarily influences mitochondria in other cellular types.
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