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. 2019 May 10;11(5):648. doi: 10.3390/cancers11050648

Figure 1.

Figure 1

Flow diagram of the study design. 2 patients’ groups (GC and AAG), as well as healthy donors (HD) were analyzed for TLR polymorphisms (rs were listed in Table 2) and serological markers for H. pylori (HP) infection. H. pylori-related pro-inflammatory interleukin (IL)-8 and IL-18 cytokines were tested in GC and in association with the respective toll-like receptor (TLR)5 and TLR9 patient’s genotype. Gastrin G-17, PG-I and H. pylori-like markers for AAG and GC risk, were tested in association with the respective TLR5 and TLR9 patient’s genotype. The flagellin A of H. pylori strains isolated from AAG and GC patients were characterized by proteomics (DIGE (differential in gel analysis) and immunoblotting) and DNA sequencing. Spot abundances for flaA identified in each single gel by DIGE and bacteria motility were matched with the TLR5 polymorphism of the respective patient. The presence of virulent CagA gene in H. pylori strains isolated from patients with GC and AAG was tested by specific-polymerase chain reaction (PCR) assay. Number of individuals studied was reported under single assay.