Chronic inflammation caused by Helicobacter pylori infection poses a major health risk because of its strong ties to gastric cancer development. This bacterium is adept at manoeuvring out of the host immune responses against it, having successfully colonized the human stomach for over 50 000 years and strategically co-evolving with its host. On the other hand, lactobacilli play an important role as a part of the normal microbiota. They protect against pathogenic infections by competing for space and nutrients, producing antimicrobial agents or directly interacting with the host cells. In Paper I, we investigated the role of Lactobacillus strains in inhibiting pro- inflammatory cytokine production in H. pylori-infected macrophages. We found that some strains but not all, were able to suppress TNF and IL-6 production in these infected cells via the ADAM17 pathway. In Paper II, we studied the potential role that lactobacilli can have in regulating ADAM17 targets in host epithelial and immune cells infected with H. pylori. We found that ADAM17-regulated proliferation markers TGF-α and HBEGF were downregulated by certain Lactobacillus strains in H. pylori-infected gastric epithelial cells, and a lower immune cell infiltration was observed in gastric tissue samples pre-treated with these lactobacilli. In Paper III, we tested the potential of certain Lactobacillus strains in regulating transcriptional factors of H. pylori, as well as the importance of these factors in motility, acid survival and antimicrobial resistance. Our findings revealed a novel role of H. pylori ferric regulator fur in surviving human cathelicidin LL-37, and also showed the ability of lactobacilli to downregulate H. pylori motility gene flgR and acid resistance gene arsS. Lastly, in Paper IV, we investigated the role that lactate has in H. pylori virulence and host immune responses. Our findings revealed that lactate causes the downregulation of H. pylori adhesin genes sabA and labA, while also dampening the production of TNF and IL-6 in the host.