Objectives
Disruption of protein synthesis, by drug‐mediated restriction of the ribosomal nascent peptide exit tunnel (NPET), may inhibit bacterial growth. Here, we have studied the secondary and tertiary structures of domain V of the 23S rRNA in the wild‐type and mutant (resistant) H. pylori strains and their mechanisms of interaction with clarithromycin (CLA).
Methods
H pylori strains, isolated from cultured gastric biopsies, underwent CLA susceptibility testing by E test, followed by PCR amplification and sequencing of domain V of 23S rRNA. The homology model of this domain in H pylori, in complex with L4 and L22 accessory proteins, was determined based on the E. coli ribosome 3D structure. The interactions between CLA and 23S rRNA complex were determined by molecular docking studies.
Results
Of the 70 H pylori strains, isolated from 200 dyspeptic patients, 11 (16%) were CLA‐resistant. DNA …