Fifteen out of 32 H. pylori isolates were cagA positive, representing 55.5% (15/27) of the isolates recovered from patients with gastritis. No strain identified from patients with NUD was cagA positive. The prevalence of the allelic variants of s1 and m1 of vacA was higher in the strains isolated from patients with gastritis compared with the strains isolated from NUD patients (77.8% versus 60%, and 63% vs 40%, respectively). When the cagA and
vacA genotypes were combined and analyzed in relation FK506 chemical structure to the clinical outcome (Table 3), the cagA + strains with the allelic variant s1m1 of vacA were only present in the strains isolated from gastritis patients (53.3%). Table 2 Prevalence of cagA and allelic variants of vacA on the H. pylori strains Gastroduodenal condition CagA VacA CagA + CagA – s1 s2 m1 m2 Gastritis * 15 (55.5%) 12
(44.5%) 21 (77.8%) 6 (22.2%) 17 (63%) 10 (37%) NUD ** 0 (0%) 5 (100%) 3 (60%) 2 (40%) 2 (40%) 3 (60%) *Strains isolated from patients with gastritis (n = 27) **Strains isolated from patients with non-ulcer dyspepsia (n = 5). Table 3 Prevalence of cagA related to the main allelic combinations of vacA Gastroduodenal condition CagA+ CagA- s1m1 s1m2 s2m2 s1m1 s1m2 s2m1 s2m2 Gastritis * 8(53.3%) 5(33.3%) 2(13.4%) 6(50%) 2(16.7%) 3(25%) 1(8.3%) NUD ** 0(0%) 0(0%) 0(0%) 1(20%) 2(40%) FRAX597 concentration 1(20%) 1(20%) *Strains isolated from patients with gastritis (n = 27) **Strains isolated from patients with non-ulcer dyspepsia (n = 5). The MIC values
of natural almond skin (NS), NS post in vitro gastric digestion (NS G) and NS post in vitro gastric plus duodenal digestion (NS G + D) against 34 H. pylori strains including 2 ATCC H. pylori strains are shown in Table 4. Results of negative controls containing DMSO (maximum 1% v/v) indicated the complete absence of inhibition of all the H. pylori strains tested (data not shown). All extracts inhibited the click here growth of both the clinical isolates and the reference strains. As expected, NS was the most effective (MIC range, 64 to 128 μg/mL), followed by NS G (MIC range, 128 to 512 μg/mL) and NS G + D (MIC range, 256 to 512 μg/mL). MIC values of 64, 128 and 256 μg/mL NS, NS G and NS G + D, respectively, inhibited the growth of 50% Ureohydrolase of the H. pylori tested strains. These results clearly confirm that all three polyphenol- rich extracts acted as good growth inhibitors against H. pylori with different virulence irrespective of the cagA and vacA status. In other words, there was no difference in the suppression of growth between the 8 H. pylori clinical isolates harboring the cagA +/vacAs1/m1 genotype, including the quality control strains (ATCC 43504 and 49503), and the other H. pylori genotypes. Table 4 Minimum inhibitory concentration of almond skin extracts against H. pylori (ATCC strains and clinical isolates) MIC range MIC 50 MIC 90 NS 64-128 64 128 NS G 128-512 128 256 NS G + D 256-512 256 512 Values are expressed as μg ml-1. NS: Natural almond skin polyphenol-rich extract.