Helicobacter pylori infection as a protective factor against multiple sclerosis risk in females

Marzena J Fabis Pedrini1, Alexandra Seewann2, Kirsten A Bennett1

  • 1Centre for Neuromuscular and Neurological Disorders, Western Australian Neuroscience Research Institute, The University of Western Australia, Sir Charles Gairdner Hospital, QEII Medical Centre, Nedlands, Australia.

Abstract

Insights

Helicobacter pylori infection may have a protective effect against multiple sclerosis (MS), particularly in females. Lower seropositivity was observed in MS patients, suggesting a potential role in disease prevention.

Area of Science:

  • Neuroimmunology
  • Microbiome-host interactions
  • Epidemiology

Background:

  • Growing evidence links Helicobacter pylori (H. pylori) infection to various diseases.
  • Previous studies on the association between H. pylori and multiple sclerosis (MS) have yielded conflicting results.

Purpose of the Study:

  • To investigate the potential association between H. pylori infection and the risk of developing multiple sclerosis.

Main Methods:

  • A case-control study involving 550 MS patients and 299 matched controls.
  • H. pylori specific IgG antibodies were detected in serum using enzyme immunoassay.
  • Clinical and demographic data were collected for all participants.

Main Results:

  • H. pylori seropositivity was lower in MS patients (16%) compared to controls (21%).
  • This trend was significant in females (14% vs 22%, p=0.027) but not in males (19% vs 20%, p=1.0).
  • Among females, H. pylori seropositivity correlated with lower disability scores; the opposite was observed in males.

Conclusions:

  • H. pylori infection might play a protective role in MS development, potentially linked to the 'hygiene hypothesis'.
  • The observed association was predominantly in females, warranting further investigation.
  • The findings suggest H. pylori could be a surrogate marker for immune system priming against autoimmune diseases.

Related Concept Videos

Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
2
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...
2
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.
1.6K
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...
37
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...
3
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.
2.9K