E. Coli Evasion Tactics Against Immune Responses

         

        Pathogenic E. coli strains, unlike their commensal counterparts in the gastrointestinal 

tract, utilise diverse mechanisms to evade both innate and acquired immune responses. 

According to Kobayashi et al. (2021), in cases of newborn meningitis and bacteremia, 

capsule polysaccharides such as K1 capsules and KpsMT2 create a barrier that prevents 

immune recognition and phagocytosis. Resistance to immune cells and antibodies is made 

possible by biofilm formation, which is facilitated by fimbriae, Ag43, and flagella (Martinson & 

Walk, 2020; Puri & Allison, 2024). Adhesion is further mediated by structures like colonisation 

factor antigens, Bfps, type 1 fimbriae, P fimbriae assembly protein C, and S fimbriae adhesion 

subunits D & E, facilitating tissue colonisation (Kobayashi et al., 2021). Antigenic variation, 

involving plasmids, transposons, and pathogenicity islands, allows evasion from host 

immunity (Kaper et al., 2004). The type III secretion system (T3SS) disrupts host cell 

functions through effectors like E. coli secreted protein F, G2, G, and valine glycine repeats 

proteins G1 (Ahmed et al., 2025). According to Martinson & Walk (2020) and Hunt (2010) 

studies, Iron acquisition via siderophores (fyuA) ensures bacterial growth, while Shiga toxins 

cause severe intestinal damage. Antibiotic resistance, notably extended-spectrum beta-

Lactamase (ESBL) production further enhances survival (Kaper et al., 2004).