Fig. 5.

Shows the interactions within the gastric epithelium during Helicobacter pylori infection and its role in ulcer formation. [A] presents the chemical structures and formulas of the bioactive compounds involved in inflammation: costunolide (C₁₅H₂0O₂), dehydrocostus lactone (C₁₅H₁₈O₂), and cynaropicrin (C₁₉H₂₂O₆). While [B] illustrates the pathogenesis sequence, H. pylori penetrates the mucous layer, alters the local pH via urease, and triggers an immune response. These include chemokine-mediated Polymorphonuclear neutrophils (PMNs) recruitment and cytokine release (IL-1β, TNFα, IL-12, and IFNγ) by activated macrophages and T-cells. These events lead to disrupted epithelial barriers and apoptosis mediated by Fas expression and cytokine signaling, whereas B cells produce specific antibodies (Immunoglobulin G (IgG) and Immunoglobulin A (IgA)).