Impact of Helicobacter pylori infection on gut microbiota

Chikara Iino1, Tadashi Shimoyama1

  • 1Department of Gastroenterology, Hirosaki University Graduate School of Medicine, Hirosaki 036-8562, Japan.

Insights

Helicobacter pylori (H. pylori) infection significantly impacts gut microbiota composition. While eradication therapy causes short-term changes, long-term H. pylori infection and treatments like antibiotics alter gut bacteria, requiring careful analysis.

Area of Science:

  • Microbiology
  • Gastroenterology
  • Microbiome Research

Background:

  • Emerging research highlights the intricate relationship between Helicobacter pylori (H. pylori) infection and the gut microbiota.
  • Many studies focus on H. pylori eradication therapy's effects, often as secondary analyses.

Purpose of the Study:

  • To review the impact of H. pylori infection and its eradication on gut microbiota composition.
  • To emphasize the need for comprehensive analysis considering confounding factors.

Main Methods:

  • Literature review of studies investigating H. pylori and gut microbiota.
  • Analysis of findings related to eradication therapy, H. pylori infection duration, and treatment side effects.

Main Results:

  • H. pylori eradication leads to rapid gut microbiota alterations, with many changes persisting long-term.
  • Antibiotics and proton pump inhibitors used in eradication contribute to short-term dysbiosis.
  • Chronic H. pylori infection alters gastric acidity, further modifying the gut microbiota.

Conclusions:

  • Gut microbiota composition is significantly influenced by H. pylori status and eradication treatments.
  • Future gut microbiota analyses require large populations and adjustment for factors like age, sex, BMI, diet, and H. pylori virulence.

Related Concept Videos

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...
622
Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

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...
785
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining.
660
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...
329
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...
696
Peptic Ulcer Disease II: Pathophysiology01:28

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.
1.0K