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. 2017 Oct 26;7:14089. doi: 10.1038/s41598-017-14372-2

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Lactate triggers a TlpC-dependent attractant response in H. pylori. Cultures of isogenic wild-type (WT) and ΔtlpC (∆TlpC) H. pylori PMSS1 were grown in BB10 overnight, treated with various concentrations of sodium L-lactate or control compounds as indicated, and then immediately filmed. Direction changes were enumerated over a 3 second period in at least 200 cells per treatment in two biological replicates. 10 mM HCl or 50 μM dipyridyl serve as known repellent and attractant response controls, respectively. Error bars represent the standard error of the mean. *p < 0.05; **p < 0.01, comparisons performed using a two-way ANOVA, followed by Tukey’s pairwise comparisons (α = 0.05). There were no significant differences in the basal behaviour between wild type and its tlpC mutant.