Intimate host attachment: enteropathogenic and enterohaemorrhagic Escherichia coli

Area of Science:

• Microbiology
• Cell Biology
• Pathogen-Host Interactions

Background:

• Enteropathogenic and enterohaemorrhagic *Escherichia coli* (EPEC/EHEC) employ a type III secretion system (TSS) to translocate effector proteins, such as Tir, into host cells.
• Tir integrates into the host plasma membrane, where it interacts with the bacterial adhesin intimin to form attaching and effacing (A/E) lesions.
• Tir is known to trigger host actin polymerization pathways, initially believed to be essential for A/E lesion formation.

Purpose of the Study:

• To review the discovery of Tir and its role in *E. coli* pathogenesis.
• To elucidate the actin polymerization pathways modulated by Tir.
• To summarize the current understanding of the physiological functions of Tir-induced actin polymerization.

Main Methods:

• Literature review of studies on Tir, type III secretion systems, and actin dynamics in *E. coli* infections.
• Analysis of experimental data linking Tir to host cell actin remodeling.
• Synthesis of findings regarding the roles of Tir-induced actin polymerization in bacterial colonization and disease.

Main Results:

• Tir translocation via TSS is a key colonization strategy for EPEC/EHEC.
• Tir triggers multiple actin polymerization pathways involving the Arp2/3 complex.
• Tir-induced actin polymerization is dispensable for A/E lesion formation but critical for colonization, in vivo fitness, and systemic disease.

Conclusions:

• The function of Tir has evolved beyond its role in A/E lesion formation.
• Tir-induced actin polymerization plays significant roles in the overall pathogenesis and colonization efficiency of EPEC/EHEC.
• Understanding these pathways offers insights into bacterial strategies for host colonization and potential therapeutic targets.