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Helicobacter pylori surface antigens comprise a diverse set of molecules, including outer membrane proteins (adhesins such as HpaA, BabA, SabA), lipopolysaccharide structures with variable and immunogenic O-antigen motifs, and secreted or peripheral enzymes associated with the bacterial cell surface. These antigens mediate key processes in infection, such as adhesion to gastric epithelial cells, biofilm formation, modulation and evasion of host immune response, and persistence in the stomach environment. The variability of these surface components, driven by phase variation and genetic diversity, underlies H. pylori's ability to colonize and cause chronic infection, and presents both challenges and opportunities for diagnostic and therapeutic targeting. They are key players in the pathogenesis of gastritis, peptic ulcers, and gastric cancer, but the term "surface antigens" is too broad for assignment to a specific structured drug target.
For candidate vaccines, mechanisms include eliciting antibody response to block adhesion (e.g., HpaA). For lipopolysaccharide antigens, mechanisms involve immune system recognition and activation or subversion.
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