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. 2019 Dec 16;10:5717. doi: 10.1038/s41467-019-13506-6

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© The Author(s) 2019

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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Fig. 1 — a H. pylori type-I, but not type-II strains, express a functional T4SS allowing for CagA phosphorylation in infected AGS cells as control. b TLR5 activation as quantified by NF-κB luciferase reporter gene assay is restricted to type-I isolates in HEK reporter cells. c CagA delivery and its phosphorylation in AGS cells require functional cagL and cagA, but not vacA, ureB and flaA genes. d TLR5 activation in HEK293 cells requires functional cagL. Recombinant flagellin (rFliC) of Salmonella was used as positive control. e, CagL and rFliC interact with TLR5 on TLR5⁺ cells as determined by immunoprecipitation with α-TLR5 antibodies. Quantitative data are shown as means ± SD. ****p < 0.0001 (one-way ANOVA). Each red dot represents a single data point. Source data are provided as a Source Data file.