دورية أكاديمية
أعرض في EDS

Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis.

التفاصيل البيبلوغرافية
العنوان: Clostridioides difficile Toxins: Host Cell Interactions and Their Role in Disease Pathogenesis.
المؤلفون: Alam MZ; Department of Pathology and Laboratory Medicine, Brody School of Medicine, East Carolina University, 600 Moye Boulevard, Greenville, NC 27858, USA., Madan R; Division of Infectious Diseases, Department of Internal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.; Veterans Affairs Medical Center, Cincinnati, OH 45220, USA.
المصدر: Toxins [Toxins (Basel)] 2024 May 24; Vol. 16 (6). Date of Electronic Publication: 2024 May 24.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101530765 Publication Model: Electronic Cited Medium: Internet ISSN: 2072-6651 (Electronic) Linking ISSN: 20726651 NLM ISO Abbreviation: Toxins (Basel) Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel : MDPI
مواضيع طبية MeSH: Clostridioides difficile*/genetics , Clostridioides difficile*/pathogenicity , Bacterial Toxins*/chemistry , Bacterial Toxins*/genetics , Bacterial Toxins*/immunology , Host Microbial Interactions*, Clostridium Infections/drug therapy ; Clostridium Infections/microbiology ; Clostridium Infections/pathology ; Gene Order ; Inflammation/pathology ; Humans ; Animals
مستخلص: Clostridioides difficile , a Gram-positive anaerobic bacterium, is the leading cause of hospital-acquired antibiotic-associated diarrhea worldwide. The severity of C. difficile infection (CDI) varies, ranging from mild diarrhea to life-threatening conditions such as pseudomembranous colitis and toxic megacolon. Central to the pathogenesis of the infection are toxins produced by C. difficile , with toxin A (TcdA) and toxin B (TcdB) as the main virulence factors. Additionally, some strains produce a third toxin known as C. difficile transferase (CDT). Toxins damage the colonic epithelium, initiating a cascade of cellular events that lead to inflammation, fluid secretion, and further tissue damage within the colon. Mechanistically, the toxins bind to cell surface receptors, internalize, and then inactivate GTPase proteins, disrupting the organization of the cytoskeleton and affecting various Rho-dependent cellular processes. This results in a loss of epithelial barrier functions and the induction of cell death. The third toxin, CDT, however, functions as a binary actin-ADP-ribosylating toxin, causing actin depolymerization and inducing the formation of microtubule-based protrusions. In this review, we summarize our current understanding of the interaction between C. difficile toxins and host cells, elucidating the functional consequences of their actions. Furthermore, we will outline how this knowledge forms the basis for developing innovative, toxin-based strategies for treating and preventing CDI.
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معلومات مُعتمدة: I01 BX004630 United States BX BLRD VA; R01 AI158451 United States AI NIAID NIH HHS
فهرسة مساهمة: Keywords: C. difficile transferase (CDT); Clostridioides difficile infection; GTPase proteins; pathogenicity locus (PaLoc); toxin A (TcdA) and toxin B (TcdB)
المشرفين على المادة: 0 (Bacterial Toxins)
0 (tcdA protein, Clostridium difficile)
0 (toxB protein, Clostridium difficile)
EC 2.4.2.31 (actin-specific ADP-ribosyltransferase, Clostridium)
تواريخ الأحداث: Date Created: 20240626 Date Completed: 20240627 Latest Revision: 20240702
رمز التحديث: 20240702
مُعرف محوري في PubMed: PMC11209539
DOI: 10.3390/toxins16060241
PMID: 38922136
قاعدة البيانات: MEDLINE
الوصف
تدمد:2072-6651
DOI:10.3390/toxins16060241