Related Experiment Video
Updated: Apr 26, 2026
08:32
Assessment of Intestinal Transcytosis of Neonatal Escherichia coli Bacteremia Isolates
Published on: February 17, 2023
1.7K
Dynamics of brush border remodeling induced by enteropathogenic E. coli
David A Shifrin1, Scott W Crawley1, Nathan E Grega-Larson1
1Department of Cell and Developmental Biology; Vanderbilt University Medical Center; Nashville, TN USA.
Gut Microbes
|July 31, 2014
Summary
Enteropathogenic Escherichia coli (EPEC) hijacks microvillar dynamics, using existing actin bundles to form pedestals. This process involves protocadherin-24 and pilus retraction, leading to actin pedestal formation in intestinal cells.
Area of Science:
- Microbiology
- Cell Biology
- Biochemistry
Background:
- Enteropathogenic Escherichia coli (EPEC) causes intestinal disease by altering host cell structure.
- EPEC infection leads to microvillar effacement and actin pedestal formation.
- The role of microvillar actin bundles in pedestal formation is not fully understood.
Purpose of the Study:
- To investigate the dynamics of microvilli during EPEC infection.
- To elucidate the mechanism by which EPEC utilizes microvillar actin for pedestal formation.
Main Methods:
- Live-cell imaging of polarized intestinal epithelial cells infected with EPEC.
- Analysis of actin dynamics and microvillar remodeling.
- Investigating the role of protocadherin-24 and EPEC bundle-forming pilus.
Main Results:
- EPEC induces long-range microvillar dynamics, pulling them towards bacterial attachment sites via protocadherin-24.
- Retraction of the EPEC bundle-forming pilus promotes directed elongation of adjacent microvilli.
- Microvilli coalesce, incorporating their actin bundles into EPEC-induced pedestals.
- Stabilizing microvillar actin bundles delays pedestal formation.
Conclusions:
- EPEC exploits pre-existing microvillar actin filaments for efficient pedestal formation.
- Microvillar dynamics and actin bundle incorporation are key steps in EPEC pathogenesis.
- Protocadherin-24 and pilus retraction are crucial mediators of EPEC-induced cellular remodeling.
More Related Videos
Related Concept Videos
01:18Bacterial Gastroenteritis
84
Bacterial gastroenteritis, characterized by diarrhea, abdominal cramps, and vomiting, is often caused by ingestion of contaminated food or water and is frequently associated with pathogenic Escherichia coli strains. These microbes exploit two principal mechanisms to inflict disease.Shiga toxin–producing E. coli, also referred to as STEC—notably O157:H7—release Shiga toxins that target ribosomes, blocking protein synthesis. The B subunit of the toxin binds the host glycolipid...
84
01:22Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal
1.8K
Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
1.8K
01:27Chemotaxis in E. coli
1.4K
Chemotaxis in Escherichia coli is a sensory-driven motility mechanism that enables bacteria to navigate chemical gradients, moving toward beneficial environments while avoiding harmful conditions. This process relies on a signal transduction system integrating external chemical cues with flagellar motor control.Chemoreceptors and Signal DetectionE. coli detects chemical gradients through methyl-accepting chemotaxis proteins (MCPs), which are membrane-bound chemoreceptors that sense attractants...
1.4K
01:23Renewal of Intestinal Stem Cells
2.7K
The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
2.7K
01:20Inflammatory Bowel Disease II: Ulcerative Colitis
27
Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal...
27