Finlay, 2010; Kaper et al., 2004). The E. coli producing pore forming toxin α-hemolysin causing bacteraemia/sepsis causes degradation of Bcl-XL protein among platelets via activating calpains (Kraemer et al., 2012). Thus, thrombocytopenia observed during sepsis caused by E. coli or related bacteria occurs due to calpain mediated degradation of antiapoptotic
Bcl-XL protein required for survival of platelets (Fig. 1). Additionally, …show more content…
coli (EHEC) responsible for serious diarrhoea with abdominal cramps, haemorrhagic colitis, and in some cases haemolytic uremic syndrome (HUS), thrombocytopenia and renal failure is considered as attaching and effacing (AE) pathogen due to its involvement in the causation of dramatic changes in host cell membrane and cytoskeleton (Frankel and Phillips, 2008). The EHEC induced AE lesions were caused due to activation of calpains via contact-dependent, type III secretion system (T3SS)-mediated injections of effectors molecules into the host cells (Lai et al., 2011). Activation of calpains causes cleavage of ezrin protein, which has been observed during cell spreading and migration (Lai et al., 2011). However enteropathogenic E.coli (EPEC) causing diarrhoea also seems to activate calpains to cause cell damage via T3SS but this is not as severe as in case