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Related Concept Videos

Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

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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...
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Tight junctions are molecular seals between cells that prevent the leaking of fluids, ions, and other small solutes across cavities and compartments in multicellular organisms. They are mainly composed of claudin and occludin transmembrane proteins, and other proteins such as tricellulin and JAM (junctional adhesion molecule). All these proteins are 4-pass transmembrane proteins, except JAM, which is a single-pass transmembrane protein belonging to the immunoglobulin superfamily. The...
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Strong contact points between adjacent cells anchor them to each other, forming tissues. Such anchoring junctions are of two types –  adherens junctions and desmosomes. Adherens junctions are abundant in tissues such as  epithelium and endothelium, forming a continuous zone of adhesion called the adhesion belt. In other tissues, such as  heart muscle, they appear as clusters, linking the cells to produce coordinated heart muscle contraction.
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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.
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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...
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Sensing of Barrier Tissue Disruption with an Organic Electrochemical Transistor
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Enteropathogenic E. coli: breaking the intestinal tight junction barrier.

Anand Prakash Singh1, Saima Aijaz1

  • 1Centre for Molecular Medicine, Jawaharlal Nehru University, New Delhi, 110067, India.

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|June 9, 2016
PubMed
Summary

Enteropathogenic E. coli (EPEC) causes infant diarrhea by injecting toxins that disrupt intestinal cells. This review details how EPEC targets tight junctions, leading to gut barrier dysfunction and fluid leakage.

Keywords:
Enteropathogenic E. coliparacellular permeability.tight junctions

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Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogenesis

Background:

  • Enteropathogenic E. coli (EPEC) is a significant cause of acute intestinal infections and watery diarrhea in infants, particularly in developing nations.
  • EPEC infection spreads via contaminated food and water, leading to severe gastrointestinal distress.
  • The precise molecular mechanisms underlying EPEC-induced diarrhea remain incompletely understood.

Purpose of the Study:

  • This review focuses on the virulence factors employed by EPEC.
  • It aims to elucidate how these factors target and disrupt the host cell tight junction complex.
  • The goal is to explain the contribution of tight junction alterations to EPEC-mediated diarrhea.

Main Methods:

  • Review of existing literature on EPEC pathogenesis and host-pathogen interactions.
  • Analysis of studies detailing EPEC effector proteins and their mechanisms of action.
  • Focus on research investigating the impact of EPEC on epithelial barrier integrity.

Main Results:

  • EPEC directly injects virulence factors into intestinal epithelial cells.
  • These effectors modulate host cell signaling pathways, causing cellular dysfunction.
  • A primary target is the tight junction complex, crucial for epithelial barrier function.

Conclusions:

  • EPEC disrupts the intestinal epithelial barrier by targeting tight junctions.
  • This disruption leads to increased paracellular permeability and fluid leakage, contributing to diarrhea.
  • Understanding these molecular mechanisms is key to developing therapeutic strategies against EPEC infections.