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. 2020 Sep 24;10:15711. doi: 10.1038/s41598-020-72594-3

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Mitochondrial accumulation of an autophagy marker in H. pylori infected AGS cells. (A) AGS cells were infected with H. pylori and harvested at indicated time points. Western blot analyses of LC3B, Beclin 1, p62 and actin in whole cell lysates. (B) Immunocytochemical analysis of LC3 in AGS cells infected by H. pylori for 12 h. The arrow indicates the LC3 dots. (C) Western blot analysis of P-STAT3^Ser727 and LC3B in cytosolic and mitochondrial fractions of H. pylori infected AGS cells. VDAC and α-tubulin were used as mitochondrial and cytoplasmic protein markers, respectively. The relative expression levels of LC3B-II from three independent experiments are presented means ± S.D. (D) Immunocytochemical analysis of LC3 in AGS cells co-cultured with H. pylori for 12 h. MitoTracker is a selective probe of mitochondria. Scale bar, 100 μm. (E) Transmission electron microscopy image of control cells and H. pylori-infected cells.