Mechanism of crosstalk between Helicobacter pylori and immune stromal cells in the development and occurrence of gastric cancer.

Helicobacter pylori (Hp) has been classified as a class I carcinogen in gastric cancer, and one of the important mechanisms by which it affects the gastric environment and promotes cancerogenesis is by triggering inflammation.Inflammatory responses caused by Hp's 'crosstalk' with various types of cells in the microenvironment of the gastric tumour play a key role in cancer progression, but the exact mechanism of its 'crosstalk' is still unclear. This paper focuses on the regulatory impact of Hp infection on the tumor microenvironment, systematically explores the activation process of immune stromal cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), mesenchymal stem cells (MSCs), and myeloid-derived suppressor cells by directly or indirectly promoting the secretion of inflammatory factors by Hp, and analyzes the molecular mechanism of these cells that influence the occurrence and development of gastric cancer through multiple signal pathways, in order to provide innovative theoretical basis for the development of accurate prevention and treatment strategies for Hp infection-related gastric cancer.