Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy

Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...

Complement System

Complement System

The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a membrane...

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.

Gastritis II: Pathophysiology

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...

Peptic Ulcer Disease II: Pathophysiology

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Trends in indications, complications and outcomes for venous resection during pancreatoduodenectomy.

The British journal of surgery·2017

Same author

Ethnicity differences in breast cancer stage at the time of diagnosis in Norway.

Scandinavian journal of surgery : SJS : official organ for the Finnish Surgical Society and the Scandinavian Surgical Society·2015

Same author

Decreasing time trend in SSI incidence for orthopaedic procedures: surveillance matters!

The Journal of hospital infection·2012

Same author

Sweet-talk: role of host glycosylation in bacterial pathogenesis of the gastrointestinal tract.

Gut·2011

Same author

The Membrane Glycoprotein IIb/IIIa Complex Mediates Deposition of Thrombin-stimulated Blood Platelets on Polystyrene Plastic Under Static Conditions.

Platelets·2010

Same author

The Fluid-phase SC5b-9 Terminal Complement Complex Binds to the GPIIb/IIIa Complex of Thrombin-stimulated Human Blood Platelets Inhibiting Platelet Aggregation.

Platelets·2010

Search research articles

Related Experiment Video

Updated: Jul 5, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

Complement activation directly induced by Helicobacter pylori.

A E Berstad¹, K Høgåsen, G Bukholm

¹Laboratory for Immunohistochemistry and Immunopathology (LIIPAT), Rikshospitalet, Institute of Pathology, N-0027 Oslo, Norway. audun.berstad@rh.uio.no

Gastroenterology

|March 27, 2001

Summary

This summary is machine-generated.

Helicobacter pylori activates the classic complement pathway via its lipopolysaccharides (LPSs), leading to bacterial sensitivity. This interaction may explain gastric pathology without mucosal invasion.

More Related Videos

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

Published on: June 18, 2016

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes

Published on: July 5, 2024

Related Experiment Videos

Last Updated: Jul 5, 2026

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

High Resolution Electron Microscopy of the Helicobacter pylori Cag Type IV Secretion System Pili Produced in Varying Conditions of Iron Availability

Published on: November 21, 2014

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

One-step Negative Chromatographic Purification of Helicobacter pylori Neutrophil-activating Protein Overexpressed in Escherichia coli in Batch Mode

Published on: June 18, 2016

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes

Profiling Luminal pH in Three-Dimensional Gastrointestinal Organoids Using Microelectrodes

Published on: July 5, 2024

Area of Science:

Immunology
Microbiology
Gastroenterology

Background:

Helicobacter pylori is a common gram-negative bacterium colonizing the human stomach.
Its interaction with the complement system may play a role in chronic gastritis pathogenesis.

Purpose of the Study:

To investigate the in vitro interaction between H. pylori and the complement system.
To determine if H. pylori activates complement via the classic pathway and its susceptibility to complement-mediated killing.

Main Methods:

Four H. pylori strains (2 cagA+, 2 cagA-) and their purified lipopolysaccharides (LPSs) were incubated with non-immune serum.
Complement activation products (C3bc and TCC) were quantified using immunoassays.
Serum sensitivity was assessed by colony-forming unit counts and bacterial morphology observation.

Main Results:

All H. pylori strains and LPSs robustly activated complement, generating significant C3bc and TCC.
Complement activation primarily occurred via the classic pathway, as indicated by reduced products when this pathway was blocked.
H. pylori demonstrated serum sensitivity, with significant bacterial killing observed in the presence of ≥30% non-immune serum, and bacteria appeared swollen and coated with complement products.

Conclusions:

H. pylori is sensitive to complement-mediated killing and activates the classic complement pathway even without specific antibodies.
Released bacterial components, particularly LPSs, can activate complement, potentially explaining H. pylori-induced gastric pathology without deep mucosal invasion.