ArticleThe Journal of biological chemistry2010
Clostridium difficile toxin A decreases acetylation of tubulin, leading to microtubule depolymerization through activation of histone deacetylase 6, and this mediates acute inflammation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 51 citations in OpenAlex.
- HDAC6 Promotes Host Defense Against Chlamydial Lung Infections by Regulating M2-Th2 Responses.International journal of molecular sciences · 2026Article
- Gut Microbiota-Gut Metabolites andMetabolites · 2024Review
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- Soluble pathogenic tau enters brain vascular endothelial cells and drives cellular senescence and brain microvascular dysfunction in a mouse model of tauopathy.Nature communications · 2023Article
- Advances in the Mechanistic Study of the Control of Oxidative Stress Injury by Modulating HDAC6 Activity.Cell biochemistry and biophysics · 2023Article
- Candida gut colonization, yeast species distribution, and biofilm production in Clostridioides difficile infected patients: a comparison between three populations in two different time periods.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2021Article
- Role of HDAC6 inhibition in sepsis-induced acute respiratory distress syndrome (Review).Experimental and therapeutic medicine · 2021Review
- MicroRNA-22 negatively regulates LPS-induced inflammatory responses by targeting HDAC6 in macrophages.BMB reports · 2020Article
- Porcine Colostrum Protects the IPEC-J2 Cells and Piglet Colon Epithelium againstMicroorganisms · 2020Article
- The Effect of Hydroxamic Siderophores Structure on Acetylation of Histone H3 and Alpha Tubulin inInternational journal of molecular sciences · 2019Article
- Trichostatin A, a Histone Deacetylase Inhibitor, Alleviates Eosinophilic Meningitis Induced byFrontiers in microbiology · 2019Article
- Dynamic localization of α-tubulin acetyltransferase ATAT1 through the cell cycle in human fibroblastic KD cells.Medical molecular morphology · 2018Article
- Crosstalk between HDAC6 and Nox2-based NADPH oxidase mediates HIV-1 Tat-induced pro-inflammatory responses in astrocytes.Redox biology · 2017Article
- Host-Microbiota Interactions in the Pathogenesis of Antibiotic-Associated Diseases.Cell reports · 2016Article
- Nitrotyrosine impairs mitochondrial function in fetal lamb pulmonary artery endothelial cells.American journal of physiology. Cell physiology · 2016Article
- Tubulin acetylation: responsible enzymes, biological functions and human diseases.Cellular and molecular life sciences : CMLS · 2015Review
- Critical roles of Clostridium difficile toxin B enzymatic activities in pathogenesis.Infection and immunity · 2015Article
- Persistence and toxin production by Clostridium difficile within human intestinal organoids result in disruption of epithelial paracellular barrier function.Infection and immunity · 2015Article
- Role of NADH: quinone oxidoreductase-1 in the tight junctions of colonic epithelial cells.BMB reports · 2014Article
- Natural indoles, indole-3-carbinol and 3,3'-diindolymethane, inhibit T cell activation by staphylococcal enterotoxin B through epigenetic regulation involving HDAC expression.Toxicology and applied pharmacology · 2014Article
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Clostridium difficile toxin A is known to cause actin disaggregation through the enzymatic inactivation of intracellular Rho proteins. Based on the rapid and severe cell rounding of toxin A-exposed cells, we speculated that toxin A may be involved in post-translational modification of tubulin, leading to microtubule instability. In the current study, we observed that toxin A strongly reduced α-tubulin acetylation in human colonocytes and mouse intestine. Fractionation analysis demonstrated that toxin A-induced α-tubulin deacetylation yielded monomeric tubulin, indicating the presence of microtubule depolymerization. Inhibition of the glucosyltransferase activity against Rho proteins of toxin A by UDP-2',3'-dialdehyde significantly abrogated toxin A-induced α-tubulin deacetylation. In colonocytes treated with trichostatin A (TSA), an inhibitor of the HDAC6 tubulin deacetylase, toxin A-induced α-tubulin deacetylation and loss of tight junction were completely blocked. Administration of TSA also attenuated proinflammatory cytokine production, mucosal damage, and epithelial cell apoptosis in mouse intestine exposed to toxin A. These results suggest that toxin A causes microtubule depolymerization by activation of HDAC6-mediated tubulin deacetylation. Indeed, blockage of HDAC6 by TSA markedly attenuates α-tubulin deacetylation, proinflammatory cytokine production, and mucosal damage in a toxin A-induced mouse enteritis model. Tubulin deacetylation is an important component of the intestinal inflammatory cascade following toxin A-mediated Rho inactivation in vitro and in vivo.
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