Fig. 7. A proposed model of cross-talk among H. pylori, gastric epithelial cells, ADM, and macrophages, leading to IFN-γ-producing T-cell responses and ADM–IFN-γ-mediated pro-inflammation in gastric mucosa during H. pylori infection.

H. pylori stimulates gastric epithelial cells to secrete ADM via PI3K–AKT signaling pathway activation in a cagA-dependent manner. Release of ADM induces the differentiation of IFN-γ-producing T cells via the phosphorylation of AKT and STAT3. On the other hand, ADM stimulates macrophages to produce IL-12, which promotes the IFN-γ-producing T-cell responses. Increased ADM and IFN-γ exert a pro-inflammatory effect within the gastric microenvironment, which collectively contributes to gastritis during H. pylori infection.