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Highly conserved type 1 pili promote enterotoxigenic E. coli pathogen-host interactions.

Alaullah Sheikh¹, Rasheduzzaman Rashu², Yasmin Ara Begum²

¹Molecular Microbiology and Microbial Pathogenesis Program, Division of Biology and Biomedical Sciences, Washington University School of Medicine, Saint Louis, Missouri, United States of America.

Plos Neglected Tropical Diseases

|May 23, 2017

Summary

Type 1 pili are crucial for enterotoxigenic Escherichia coli (ETEC) virulence. These pili, along with colonization factors, enhance bacterial adhesion and toxin delivery to intestinal cells, impacting diarrheal illness.

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Area of Science:

Microbiology
Pathogenesis
Bacterial Adhesion

Background:

Enterotoxigenic Escherichia coli (ETEC) cause diarrheal illness by delivering toxins to host enterocytes.
ETEC utilize adhesins and colonization factors for host cell engagement.
Type 1 pili expression is upregulated upon contact with intestinal epithelia.

Purpose of the Study:

To investigate the role of type 1 pili in ETEC adhesion and toxin delivery.
To determine if type 1 pili contribute to ETEC virulence in model systems.

Main Methods:

Studied ETEC adhesion to cultured intestinal epithelium and human small intestinal stem cell-derived monolayers.
Investigated the function of the FimH adhesin on type 1 pili.
Utilized soluble mannose, anti-FimH antibodies, and fimH mutagenesis to block interactions.
Assessed toxin delivery in vitro and virulence in rabbit ileal loop assays.

Main Results:

Type 1 pili, encoded in the E. coli core genome, are essential for ETEC virulence.
Type 1 pili act with plasmid-encoded colonization factors for optimal adhesion.
FimH-mediated adhesion is dependent on mannosylated proteins on host cells.
fimH mutants showed impaired toxin delivery and reduced virulence in vivo.

Conclusions:

Conserved type 1 pili play a critical role in the virulence of diverse ETEC strains.
Type 1 pili are key mediators of ETEC-host cell interactions and subsequent pathogenesis.