THE MOLECULAR BATTLE FIELD: HOST PATHOGEN INTERACTIONS IN H. PYLORI INDUCED GASTRIC DISEASE

Abstract

Background:

Helicobacter pylori is a usual bacterium of the stomach that has been linked to chronic inflammation of the stomach lining, the formation of stomach ulcers, instability of the stomach's inner lining, and cancer of the stomach. Gastric diseases H. pylori cause cannot be attributed to the colonization of the bacterium alone.

Objective:

This thesis review aimed to analyze the existing literature on host–pathogen interactions in the context of H. pylori-induced gastric disease, with particular emphasis on bacterial virulence, host defense, molecular mechanisms, and disease development.

Methodology:

This research was executed via a systematic literature review. Pouring through articles that had been fully accessed and had completed peer review from a number of reliable databases: Scopus, Web of Science, PubMed, and Google Scholar.  Throughout the process, 120 articles that had been published between the years of 1984 and 2025 were sourced, then further narrowed down to 75

Results:

The examined research explains that H. pylori affects the stomach tissue using a number of integrated techniques. Epithelial injury, inflammation, and malignant transformation, as well as altered autophagy and mitochondrial dysfunction, are caused by CagA, VacA, and the cag-T4SS complex. CagA, VacA, and the Cag-T4SS complex, among others, also assist in immunoactivation, inflation signal and dysbiosis of microbiota.

Conclusion:

This review found that Helicobacter pylori-initiated gastric ailments are poly-descriptive diseases that entail endless reciprocal relationships of the microbial virulence and host molecular mechanisms. In Pakistan, integrated molecular frameworks research are urgently warranted to refine the early diagnostics, risk stratification, tailored interventions, and gastro cancer prophylaxis