Resent studies reported that aspirin inhibited the growth of H. pylori in a dose-dependent manner and significantly affected the activity of virulence factors of H. pylori. In addition, aspirin increased the susceptibility of H. pylori to antimicrlbials including metronidazole, clarithromycin and amoxicillin. However, the mechanisms remained unknown.
A research team led by Prof. Wang from Peking University First Hospital of China addressed this issue.
H. pylori reference strain 26695 and two metronidazole-resistant isolates of H. pylori were included in this study. The effect of aspirin on the permeability of the outer membrane of H. pylori was determined using [7-3H] tetracycline. The effects of aspirin on the expression of OMPs of H. pylori were also determined. Taqman-based real-time quantitative PCR was used to analyze the influence of aspirin on the expression of the related OMPs genes.
They found that the mutations in rdxA gene did not change in metronidazole resistant isolates treated with aspirin. The radioactivity of H. pylori increased when treated with aspirin, indicating that aspirin improved the permeability of the outer membrane of H. pylori. However, the expression of two OMP bands between 55 kDa and 72 kDa altered in the presence of aspirin. The expression of the mRNA of hopA, hopB, hopC, hopD, hopE and hefA, hefB, hefC of H. pylori did not change when treated with aspirin.
Their results indicated that although aspirin increases the susceptibility of H. pylori to metronidazole, it has no effect on the mutations of rdxA gene of H. pylori. Aspirin increases endocellular concentrations of antimicrobials and probably by altering the expression of the outer membrane proteins (OMP) of H. pylori. Their study will help understand the mechanisms of the resistance of H. pylori to antibiotics more intensively and discover a more effective eradication regimen in clinical practice.
- Zhang et al. Aspirin increases susceptibility of Helicobacter pylori to metronidazole by augmenting endocellular concentrations of antimicrobials. World Journal of Gastroenterology, 2009; 15 (8): 919 DOI: 10.3748/wjg.15.919
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