# A Narrative Review on the Multifaceted Roles of Galectins in Host–Pathogen Interactions During Helicobacter pylori Infection

## TL;DR

This review explores how galectins influence interactions between the body and Helicobacter pylori, a bacterium linked to stomach diseases and cancer.

## Contribution

The paper synthesizes current knowledge on galectins' roles in H. pylori infection, highlighting their dual effects and therapeutic potential.

## Key findings

- Galectins modulate immune responses and epithelial integrity during H. pylori infection.
- They contribute to both host defense and bacterial persistence, affecting inflammation and cancer risk.
- Galectin pathways may serve as biomarkers and therapeutic targets for H. pylori-related diseases.

## Abstract

Helicobacter pylori infection represents one of the most prevalent and persistent bacterial infections worldwide, closely linked to a spectrum of gastroduodenal diseases, including chronic gastritis, peptic ulceration, and gastric cancer. Recent advances have shed light on the critical role of endogenous lectins, particularly galectins, in modulating host–pathogen interactions within the gastric mucosa. Galectins are β-galactoside-binding proteins with highly conserved structures but diverse biological functions, ranging from regulation of innate and adaptive immunity to modulation of cell signaling, apoptosis, and epithelial integrity. This review provides a comprehensive synthesis of current knowledge on the involvement of key galectin family members—especially Galectin-1, -2, -3, -8, and -9—in the context of H. pylori infection. Their dual roles in enhancing mucosal defense and facilitating bacterial persistence are examined along with their contributions to immune evasion, inflammation, and gastric carcinogenesis. Understanding the interplay between galectins and H. pylori enhances our knowledge of mucosal immunity. This interaction may also reveal potential biomarkers for disease progression and identify novel therapeutic targets. Modulating galectin-mediated pathways could improve outcomes in H. pylori-associated diseases.