Gene polymorphisms of pathogenic Helicobacter pylori in patients with different types of gastrointestinal diseases

Figure 1 Pathogenic factors of Helicobacter pylori strains.

Figure 2 Analysis of flaA promoter spacer mutants reveals dependency of promoter activity on spacer length and supercoiling. A: Detection of flaA, flaB, topA, gyrA, gyrB, and flaR transcript abundance by RT-PCR for wild-type flaA promoter (13n), 11n 12n, 14n, and 15n spacer mutants, grown with and without novobiocin. Result of RT-PCR of 16S rRNA is shown to permit comparisons of mRNA quantity. Quantitation of flaA and flaB transcript levels (AnalySIS software, Soft Imaging Systems) is shown in (B) and (C).

Figure 3 Genomic locations of the babA, babB, and babC genes in strains J99, 26695, and HPAG1. CT: CT dinucleotide repeats.

Figure 4 Model for the role of Helicobacter pylori T4SS effector proteins in host cell interaction and disease-associated signal transduction.

Figure 5 Eight variable regions in cagPAI sequences of Chinese Helicobacter pylori strains.