Skip to main content
. Author manuscript; available in PMC: 2014 Nov 1.
Published in final edited form as: Cell Microbiol. 2013 Jul 15;15(11):1896–1912. doi: 10.1111/cmi.12158

Figure 4. HopQ triggers cagPAI dependent host cell signal transduction pathways.

Figure 4

(A) Infection time course (0–225 min) with WT, P12ΔhopQ mutant and P12ΔcagPAI (MOI 100). Activation of NF-κB was assessed by nuclear p65 translocation. Numbers of activated cells are given as a percentage of total cell number. (B) Activation of pro-inflammatory pathways in AGS cells upon infection with the H. pylori wild type strain P12 (WT), P12ΔhopQ and P12ΔcagPAI mutants in comparison to non-infected AGS cells (NI). Immunoblot analysis showing activation of MAPK JNK1/2, p38, and ERK1/2. Blots are representative of three independent experiments. (C) Production of IL-8 estimated by ELISA; NI, non-infected AGS cells. Errors bars in A and C show ± SD of three independent experiments.