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. 2021 Oct 15;89(11):e00407-21. doi: 10.1128/IAI.00407-21

FIG 8.

FIG 8

Silencing of MyD88 and IRF7 abrogated the H. pylori DNA infection-induced activation of pDCs and increased secretion of IFN-α. (A) Western blot analysis of MyD88 and IRF7 protein levels in the gastric corpus samples from uninfected (UI) mice and mice infected with H. pylori for 2, 4, or 6 months. **, P < 0.01 versus UI. N = 5 per group. (B) Western blot analysis of MyD88 and IRF7 protein levels in pDCs from mice infected with H. pylori. The percentages of CD80 and CD86 on the surfaces of pDCs determined by flow cytometry (C), IFN-α mRNA levels determined by qRT-PCR analysis (D), and IFN-α levels determined by ELISA (E) in mouse pDCs transfected with MyD88 siRNA, IRF7 siRNA, or scramble siRNA in the absence or presence of H. pylori DNA. ##, P < 0.01 versus Ctrl; $$, P < 0.01 versus scramble siRNA; &&, P < 0.01 versus MyD88 siRNA; %%, P < 0.01 versus IRF7 siRNA. The experiments were repeated independently three times.