Pfannkuch, L., Hurwitz, R., Trauisen, J., Sigulla, J., Poeschke, M., Matzner, L., Kosma, P., Schmid, M. and Meyer, T.F. (2019), ADP heptose, a novel pathogen‐associated molecular pattern identified in Helicobacter pylori. Faseb, 33: 9087‐9099. doi:10.1096/fj.201802555R.

It has come to the authors’ attention that the H. pylori P12ΔrfaD mutant described in this paper is in fact a double mutant for P12ΔrfaE/ΔrfaD. The kanamycin cassette used to replace the gene 0859 (rfaD) also disrupts the starting methionine of the gene 0858 (rfaE). The loss of the rfaE gene explains the observed phenotype, that is, lack of NF‐κB activation after H. pylori infection (shown in Figure 4B), despite an intact type IV secretion system able to translocate CagA (shown in the Supplementary Figure 5B).

Pfannkuch, L.、Hurwitz, R.、Trauisen, J.、Sigulla, J.、Poeschke, M.、Matzner, L.、Kosma, P.、Schmid, M. 和 Meyer, TF (2019), ADP heptose,在幽门螺杆菌中发现的一种新的病原体相关分子模式 。法塞布，33：9087-9099。doi:10.1096/fj.201802555R。

引起作者注意的是，本文描述的幽门螺杆菌P12 ΔrfaD突变体实际上是P12ΔrfaE/ΔrfaD的双突变体。用于替换基因 0859 (rfaD)的卡那霉素盒也破坏了基因 0858 ( rfaE)的起始蛋氨酸。rfaE基因的缺失解释了观察到的表型，即幽门螺杆菌感染后缺乏 NF-κB 活化（如图 4B 所示），尽管完整的 IV 型分泌系统能够转移 CagA（如补充图 5B 所示） ）。