Figure 6. CagY-mediated loss of T4SS function promotes bacterial persistence during an intense inflammatory response.

(A) Il10−/− mice inoculated with H pylori PMSS1 showed significantly increased gastritis compared to WT mice 4 weeks PI. (B) H pylori bacterial burden was significantly higher in WT compared to Il10−/− mice. By 4 weeks PI, bacterial burden in Il10−/− mice was frequently near the level of detection and 3 mice were uninfected (not shown). Mice whose CFU are shown in brackets yielded the colonies whose IL8 induction is shown in brackets in panel C. (C) Loss of the capacity to induce IL8 associated with changes in cagY PCR RFLP (open circles) was more apparent in H pylori colonies recovered from Il10−/− compared to WT mice, particularly in colonies from mice that showed colonization density that resembled that in WT mice. All colonies whose IL8 induction is shown in brackets in panel C were recovered from the mice whose CFU are bracketed in panel B. (D) Average normalized IL8 induction of all colonies from each mouse showed a strong inverse correlation with bacterial burden (R²=0.78, P≤0.0001). **P≤0.01,***P≤0.001.