Effect of CD14 promoter polymorphism and H. pylori infection and its clinical outcomes on circulating CD14

J Karhukorpi1, Y Yan, S Niemela

  • 1Department of Medical Microbiology, University of Oulu, Finland. jari.karhukorpi@oulu.fi

Insights

Serum soluble CD14 (sCD14) levels are influenced by genetic variations in the CD14 gene promoter and Helicobacter pylori infection. Both factors, along with gastric mucosal lesions, contribute to elevated sCD14 levels.

Area of Science:

  • Immunology
  • Genetics
  • Gastroenterology

Background:

  • CD14 is a key pattern recognition receptor involved in innate immunity.
  • Soluble CD14 (sCD14) circulates in serum and its levels can be affected by genetic and environmental factors.
  • Lipopolysaccharide (LPS) is a well-known ligand for CD14.

Purpose of the Study:

  • To investigate the impact of CD14 gene promoter polymorphism (-159C/T) and Helicobacter pylori infection on serum sCD14 levels.
  • To compare sCD14 levels in dyspeptic patients and healthy controls.
  • To identify other factors influencing sCD14 levels in dyspeptic patients.

Main Methods:

  • Serum sCD14 levels were measured using enzyme immunoassay (EIA).
  • CD14 genotyping was performed using PCR.
  • Helicobacter pylori infection was detected via serology, culture, or PCR.
  • Patient groups included dyspeptic individuals undergoing gastroscopy and healthy staff members.

Main Results:

  • Subjects with the T allele (CT or TT genotype) of the CD14 promoter polymorphism had elevated sCD14 levels compared to CC genotype.
  • H. pylori-positive individuals showed a trend towards higher sCD14 levels.
  • Dyspeptic patients with gastric ulcers, erosions, or duodenal ulcers had significantly higher sCD14 than those with normal findings or gastritis.
  • NSAID use was also associated with increased sCD14.

Conclusions:

  • Both genetic factors (CD14 promoter polymorphism) and environmental factors (H. pylori infection, mucosal lesions) significantly impact serum sCD14 levels.
  • sCD14 may serve as a potential biomarker for certain gastrointestinal conditions and infections.
  • Further research is warranted to explore the clinical implications of these findings.

Related Concept Videos

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...
Peptic Ulcer Disease III: Clinical Manifestations and Diagnostic Studies01:28

Peptic 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.
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...
Peptic Ulcer01:27

Peptic 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...
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy01:16

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...
Peptic Ulcer Disease I: Introduction01:30

Peptic Ulcer Disease I: Introduction

Peptic Ulcer Disease (PUD) is characterized by mucosal excavation in the esophagus, stomach, pylorus, or duodenum. It can manifest as acute or chronic based on the extent and duration of mucosal involvement.
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...