The present study was aimed at modifying the original formulation of Commercial Eugon agar (CEA) to develop a new H. pylori growth medium. Initial studies were carried out to determine the number of H. pylori colonies recovered on in-house H. pylori agar (IHPA), IHPA without L-cysteine and sodium sulfite (IHPA-NC), IHPA without L-cysteine (IHPA-C), IHPA without sodium sulfite (IHPA-N) and CEA as the control. Significant differences (P < 0.001) in the number of colonies recovered were observed between IHPA-N, IHPA-NC and IHPA-C. Incorporation of sodium sulfite decreased the number of colonies recovered, indicating that sodium sulfite was inhibitory to H. pylori growth. Removal of L-cysteine reduced the number of colonies recovered, suggesting that L-cysteine is necessary for the growth of H. pylori. In the subsequent study, incorporation of K(2)HPO(4) further increased the number of colonies recovered compared with IHPA-N (P < 0.001), and 0.25% (w/v) of K(2)HPO(4) yielded the highest numbers of colonies (P < or = 0.04). Finally, thirty other H. pylori clinical isolates were evaluated for their growth in the IHPAP-N, a new medium consisting of 1.5% (w/v) pepticase, 0.5% (w/v) peptone, 0.4% (w/v) sodium chloride, 0.03% (w/v) L-cysteine, 0.55% (w/v) dextrose, 0.25% (w/v) K(2)HPO(4) and 1.5% (w/v) agar. The number of colonies recovered in IHPAP-N was significantly (P < 0.005) higher than that of CEA. IHPAP-N with 0.25% K(2)HPO(4) and without sodium sulfite were adequate solid media for the growth of H. pylori.
Helicobacter pylori colonizes the gastric epithelial cells of at least half of the world's population, and it is the strongest risk factor for developing gastric complications like chronic gastritis, ulcer diseases, and gastric cancer. To successfully colonize and establish a persistent infection, the bacteria must overcome harsh gastric conditions. H. pylori has a well-developed mechanism by which it can survive in a very acidic niche. Despite bacterial factors, gastric environmental factors and host genetic constituents together play a co-operative role for gastric pathogenicity. The virulence factors include bacterial colonization factors BabA, SabA, OipA, and HopQ, and the virulence factors necessary for gastric pathogenicity include the effector proteins like CagA, VacA, HtrA, and the outer membrane vesicles. Bacterial factors are considered more important. Here, we summarize the recent information to better understand several bacterial virulence factors and their role in the pathogenic mechanism.
Matched MeSH terms: Helicobacter pylori/growth & development