Related Experiment Video
Updated: Jul 1, 2026
07:43
Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Interleukin-18 and gestosis: correlation with Helicobacter pylori seropositivity
Agostino Pugliese1, Tiziana Beltramo, Tullia Todros
1Department of Medical and Surgical Sciences, Teaching of Clinical Virology in Post Doctoral School of Infectious Disease, Amedeo di Savoia Hospital, University of Turin, Italy. agostino.pugliese@unito.it
Cell Biochemistry and Function
|September 9, 2008
Summary
Helicobacter pylori infection, particularly Cag-A strains, may be linked to pre-eclampsia (PE). While interleukin-18 (IL-18) levels were similar, H. pylori seropositivity was significantly higher in PE patients.
Area of Science:
- Obstetrics and Gynecology
- Infectious Diseases
- Immunology
Background:
- Pre-eclampsia (PE) is a serious pregnancy complication.
- The role of infections in PE pathogenesis is under investigation.
- Interleukin-18 (IL-18) is a cytokine implicated in inflammatory processes.
Purpose of the Study:
- To investigate the correlation between pre-eclampsia (PE), Helicobacter pylori (H. pylori) seropositivity, and IL-18 levels.
- To explore the potential involvement of pathogenic H. pylori strains in PE development.
Main Methods:
- Assessed IL-18 levels using ELISA in 25 pre-eclamptic and 25 healthy pregnant women.
- Determined H. pylori seropositivity via anti-IgG ELISA.
- Detected anti-Cag-A antibodies using an immunoblot assay.
Main Results:
- No significant difference in IL-18 levels was observed between PE patients and healthy controls (350 ± 150 vs. 399 ± 132 pg/mL, p=0.23).
- H. pylori seropositivity was significantly higher in PE patients (84%) compared to controls (32%, p<0.001).
- Presence of anti-Cag-A antibodies was also significantly higher in PE patients (80%) versus controls (28%).
Conclusions:
- H. pylori infection, especially from Cag-A strains, is hypothesized to play a role in some cases of pre-eclampsia.
- H. pylori may modulate IL-18 release, contributing to PE pathogenesis.
- Further research is needed to elucidate the mechanisms linking H. pylori infection and PE.
Related Concept Videos
01:26Gastritis 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...
01:17Gastritis-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...
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...
01:27Peptic Ulcer
Peptic ulcers are erosive lesions of the gastric or duodenal lining, most commonly caused by Helicobacter pylori infection. This Gram-negative, helical bacterium has adapted to survive the stomach’s acidic environment by producing urease, which converts urea into ammonia and carbon dioxide. The ammonia neutralizes gastric acid in the bacterium’s immediate environment, allowing colonization of the gastric mucosa. H. pylori attaches to mucus-secreting epithelial cells, penetrates the mucus...
01:28Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies
Peptic ulcer disease (PUD) presents with diverse symptoms depending on the location and severity of the ulcer. Clinical manifestations of peptic ulcer include dull pain and a burning sensation in the mid-epigastric region.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
Few clinical manifestations differentiate gastric ulcers from duodenal ulcers. Distinctions in the location, timing, and pain relief are crucial for healthcare providers in differentiating between gastric and duodenal ulcers during clinical assessments.
01:24Peptic 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...
01:22Pathophysiology 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...
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...