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Clostridioides difficile toxins, primarily Toxin A (TcdA) and Toxin B (TcdB), are the principal virulence factors responsible for the pathogenesis of C. difficile infection (CDI). These large clostridial toxins function as glucosyltransferases that target and inactivate Rho-family GTPases within host colonic epithelial cells, leading to massive cytoskeleton reorganization, cell death, and loss of intestinal barrier integrity (Source: StatPearls, NBK431054). The resulting inflammatory response and tissue damage manifest clinically as diarrhea and colitis. Therapeutic strategies targeting these toxins include monoclonal antibodies like Bezlotoxumab, which binds to TcdB to prevent its entry into host cells, thereby reducing the risk of CDI recurrence (Source: FDA Label). Other microbial antigens, such as the binary toxin (CDT) and surface layer proteins, are also investigated as targets for diagnostic assays and vaccine development to provide broader protection against hypervirulent strains (Source: PMID: 30139805).
Monoclonal antibodies bind to and neutralize the toxins, preventing their attachment to host cell receptors and subsequent internalization, thereby protecting the colonic epithelium from damage (Source: PMID: 28099828). Vaccines targeting these antigens induce an immune response to produce endogenous neutralizing antibodies (Source: PMID: 29107561).
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