A broad overview of enteric pathogenic E. coli and the diseases they cause can be found elsewhere (Croxen et al., 2013). This review focuses on effectors that impact these innate immune pathways, defining host cellular targets, providing mechanistic details and describing the outcomes of effector activity. coli (CR REPEC) (Deng et al., 2004).ĮPEC and EHEC are able to overcome host innate immune defences via the action of T3SS-secreted effectors, which empower EPEC/EHEC to block phagocytosis and manipulate both inflammatory and cell survival pathways (Table 1). T3SS and its effectors are essential components of the A/E pathogen infection strategy, and are crucial for infection by EPEC/EHEC, the mouse pathogen Citrobacter rodentium and rabbit enteropathogenic E.

These effectors target host cellular signalling pathways, including those involved in cytoskeletal rearrangements, vesicle trafficking and cell survival (Croxen et al., 2013). Like many other enteric pathogens, they utilize a syringe-like type III secretion system (T3SS) to translocate effector proteins into host cells, which facilitate bacterial colonization, survival and immune evasion in infected hosts (Deng et al., 2004 Croxen et al., 2013). Once activated, the innate immune response mediates the control of invading pathogens, the induction of programmed cell death in infected host cells, and the secretion of pro-inflammatory compounds that recruit immune cells to sites of infection (Mogensen, 2009 Takeuchi and Akira, 2010).Įnteropathogenic and enterohaemorrhagic Escherichia coli (EPEC EHEC) are Gram-negative, attaching and effacing (A/E) pathogens that infect human IECs (Croxen et al., 2013). The innate immune response represents the first active line of defence against enteric pathogens, and intestinal epithelial cells (IECs) coordinate this response to combat incoming pathogenic microorganisms (Mogensen, 2009). The intestinal epithelium is a crucial component of immune defence, providing a physical barrier between the body and the outside environment (Kato et al., 2014).

Subversion hosts