Clostridium difficile toxin B induces senescence in enteric glial cells: A potential new mechanism of Clostridium difficile pathogenesis

In conclusion, TcdB induces senescence in EGCs. The extrapolation of these results to CDI leads to hypothesize that EGC that survived TcdB, once they have acquired a senescence state, could cause IBS and IBD due to persistent inflammation, transfer of senescence status and stimulation of pre-neoplastic cells.Graphical abstractToxin B f C. difficile (TcdB) induces in enteric glial cells (EGC) a senescence phenotype, which is dependent on p27 overexpression and activation of AKT and JNK, but independent on the p16/pRb and p53/p21 pathways as well as ROS. In callout are reported the main events induced by TcdB.
Source: Biochimica et Biophysica Acta (BBA) Molecular Cell Research - Category: Molecular Biology Source Type: research