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Abstract Helicobacter pylori increases risk of gastric diseases including gastric cancer. Despite development of a robust immune response,H .pylori persists in the gastric niche. Progression of gastric inflammation to serious disease outcomes is associated with infection withH .pylori strains which encode thecag Type IV Secretion System (cag T4SS). Thecag T4SS is responsible for translocating the oncogenic protein CagA into host cells and inducing pro‐inflammatory and carcinogenic signaling cascades. Our previous work demonstrated that nutrient iron modulates the activity of the T4SS and biogenesis of T4SS pili. In response toH .pylori infection, the host produces a variety of antimicrobial molecules, including the iron‐binding glycoprotein, lactoferrin. Our work shows that apo‐lactoferrin exerts antimicrobial activity againstH .pylori under iron‐limited conditions, while holo‐lactoferrin enhances bacterial growth. CulturingH .pylori in the presence of holo‐lactoferrin prior to co‐culture with gastric epithelial cells, results in repression of thecag T4SS activity. Concomitantly, a decrease in biogenesis ofcag T4SS pili at the host‐pathogen interface was observed under these culture conditions by high‐resolution electron microscopy analyses. Taken together, these results indicate that acquisition of alternate sources of nutrient iron plays a role in regulating the pro‐inflammatory activity of a bacterial secretion system and present novel therapeutic targets for the treatment ofH .pylori ‐related disease.