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Mw: 270 kD
Clostridioides (Clostridium) difficile toxin B (TcdB) induces neurogenic inflammation by targeting gut-innervating afferent neurons and pericytes through receptors, including the Frizzled receptors (FZD1, FZD2 and FZD7) in neurons and chondroitin sulfate proteoglycan 4 (CSPG4) in pericytes.
Clostridioides (Clostridium) difficile toxin B (TcdB) stimulates the secretion of the neuropeptides substance P (SP) and calcitonin gene-related peptide (CGRP) from neurons and pro-inflammatory cytokines from pericytes.
Targeting neurogenic inflammation provides a host-oriented therapeutic approach for treating Clostridioides difficile infection (CDI).
Residue variations within this region divide major Clostridium difficile (today named Clostridioides difficile) Toxin B (TcdB) variants into two classes: one recognizes Frizzled (FZD), and the other recognizes TFPI.
The four functional domains of Clostridium (today named Clostridioides) difficile toxin A (TcdA) include the glucosyltransferase domain (GTD) (red), auto-protease domain (APD) (blue), delivery domain (yellow), and combined repetitive oligo-peptides (CROPS) domain (gray).
Mileto et al. 2019 Microbiol Spectrum 7(3): GPP3- 0015-2018
These toxins (Bacteria & Toxins), despite their functional and structural similarity, do not contribute to disease equally
Mileto et al. 2019 Microbiol Spectrum 7(3): GPP3- 0015-2018
Clostridium (today named Clostridioides) difficile toxin B (TcdB) is a member of the large clostridial glucosylating toxin family, members of which are also found in several other Pathogenic clostridia .
The C-terminal end of Clostridium (today named Clostridioides) difficile toxin B (TcdB), consisting of the combined repetitive oligo-peptides (CROPS) domain, is thought to facilitate receptor binding for the toxin.
Supposedly, the toxin B of C. difficile (tcdB) deregulates Rho-GTPases, leading to increased expression of Proto-Oncogenes.
see also:
Clostridioides (Clostridium) difficile toxins & Members