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Related Concept Videos

Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Bacterial Gastroenteritis01:18

Bacterial Gastroenteritis

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 receptor...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...

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Enteric Bacterial Invasion Of Intestinal Epithelial Cells In Vitro Is Dramatically Enhanced Using a Vertical Diffusion Chamber Model
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Enteric Bacterial Invasion Of Intestinal Epithelial Cells In Vitro Is Dramatically Enhanced Using a Vertical Diffusion Chamber Model

Published on: October 22, 2013

Campylobacter jejuni-mediated disease pathogenesis: an update.

Matthias Zilbauer1, Nick Dorrell, Brendan W Wren

  • 1Infectious Diseases and Microbiology Unit, Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK. m.zilbauer@ich.ucl.ac.uk <m.zilbauer@ich.ucl.ac.uk>

Transactions of the Royal Society of Tropical Medicine and Hygiene
|November 21, 2007
PubMed
Summary

Campylobacter jejuni infection causes widespread diarrheal disease, especially in young children. Recent genomic insights are advancing our understanding of its pathogenesis and host immune responses.

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Area of Science:

  • Microbiology
  • Immunology
  • Infectious Diseases

Background:

  • Campylobacter jejuni is the leading cause of bacterial diarrhea globally.
  • Young children are the most susceptible population to C. jejuni infections.
  • Severe post-infectious complications, like Guillain-Barré syndrome, can arise.

Purpose of the Study:

  • To highlight recent advancements in C. jejuni research.
  • To focus on disease pathogenesis and early host immune responses.
  • To explore the role of glycosylation systems in bacterial virulence.

Main Methods:

  • Genomic sequence analysis of various C. jejuni strains.
  • Investigation of bacterial glycosylation systems (O- and N-linked).
  • Review of current literature on host-pathogen interactions.

Main Results:

  • Genome sequencing has accelerated research into C. jejuni genetics and pathogenesis.
  • C. jejuni possesses unique O- and N-linked glycosylation systems.
  • These systems likely influence bacterial virulence, survival, and host interactions.

Conclusions:

  • Understanding C. jejuni pathogenesis is crucial due to its significant health burden.
  • Glycosylation systems represent a key area for modulating virulence and host response.
  • Further research is needed to fully elucidate host immunity and disease mechanisms.