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<i>Helicobacter pylori</i> infection triggers inflammation that may lead to gastritis, stomach ulcers and cancer. Probiotic bacteria, such as <i>Lactobacillus</i>, have been of interest as treatment options, however, little is known about the molecular mechanisms of <i>Lactobacillus</i>-mediated inhibition of <i>H. pylori</i> pathogenesis. In this work, we investigated the effect of <i>Lactobacillus</i> culture supernatants, so-called conditioned medium (CM), from two gastric isolates, <i>L. gasseri</i> and <i>L. oris</i>, on the expression of transcriptional regulators in <i>H. pylori</i>. Among the four known two-component systems (TCSs), i.e., ArsRS, FlgRS, CheAY and CrdRS, the flagellar regulator gene <i>flgR</i> and the acid resistance associated <i>arsS</i> gene were down-regulated by <i>L. gasseri</i> CM, whereas expression of the other TCS-genes remained unaffected. <i>L. gasseri</i> CM also reduced the motility of <i>H. pylori</i>, which is in line with reduced <i>flgR</i> expression. Furthermore, among six transcription factors of <i>H. pylori</i> only the ferric uptake regulator gene <i>fur</i> was regulated by <i>L. gasseri</i> CM. Deletion of <i>fur</i> further led to dramatically increased sensitivity to the antimicrobial peptide LL-37. Taken together, the results highlight that released/secreted factors of some lactobacilli, but not all, downregulate transcriptional regulators involved in motility, acid tolerance and LL-37 sensitivity of <i>H. pylori</i>.