![]() Inoculated Mongolian gerbils were sacrificed after 1 month (TN2-1M), 3 months (TN2-3M), and 6 months (TN2-6M). No specific pretreatments were administered prior to orogastric H. pylori (10 9 colon-forming units/mL) or sterile brain–heart infusion (BHI) broth using gastric intubation needles after 16 h of fasting. Six-week-old male Mongolian gerbils (MGS/Sea Harlan Sprague Dawley) were orogastrically inoculated 3 times (days 0, 1, 2) with 1.0 mL of H. We inoculated TN2 wild type strain (TNwt) to Mongolian gerbils as described in our previous paper. Inoculation, euthanasia and isolation of H. We detected mutations in agreement with previous studies and identified new mutations that may be associated with adaptation of the bacteria to different hosts. Here, we used the whole genome sequence of TN2 wild type (TN2wt) as a reference and sequenced short reads from three derivative strains to identify genomic mutations during infection in Mongolian gerbils. However, DNA sequencing advancements enabled the extensive exploration of mutations by sequencing bacterial genomes before and after infection. Įarlier studies used PCR to investigate changes in genes during animal infection. pylori initially increased upon infection but reduced over time, then lost after 6 months and that infection with oipA or babA mutants resulted in significantly reduced cytokine levels but alpAB mutant did not infect Mongolian gerbils. We also used Mongolian gerbils as the model animal and discovered that babA expression in H. Thus, they work as the good animal model. pylori infection as gastric inflammation, ulceration and cancer. Small rodent Mongolian gerbils develop similar symptoms to human by H. Model animals are expected to respond to the stimulation in the similar manner to humans and be maintained on reasonable cost and handling efforts. pylori in the infected animals was also studied. In search of a good animal model, experimental infection was attempted in Rhesus monkeys, mice, and Mongolian gerbils. ![]() pylori is well adapted to the human stomach but does not easily infect other animals. pylori in the time course of chronic infection or transmission and revealed that the mutation rate of this bacterium is high. Previous studies investigated genetic diversification of H. pylori) is known to a risk factor of various gastrointestinal diseases. We also listed up genes that mutated during the infection to the gerbils, though it needs experiments to prove the influence on adaptation. ![]() We confirmed mutations in genes previously reported to be associated with adaptation to Mongolian gerbils. Other mutations were involved with chemoreceptor, pH regulator, and outer membrane proteins, which also have potential to influence on the adaptation to the new host. Mutated genes included babA, tlpB, and gltS, which are known to be associated with adaptation to murine. Multiple mutations were observed in three genes. Missense and nonsense mutations were observed in 15 and 6 loci, respectively. Of the 17 genes, five were outer membrane proteins that potentially influence on the colonization and inflammation. We identified mutations in 21 loci of 17 genes of the post-inoculation strains. pylori after infection in Mongolian gerbils, we compared the whole genome sequence of TN2 wild type strain (TN2wt) and next generation sequencing data of retrieved strains from the animals after different lengths of infection. pylori may accumulate mutations to adapt to the new host. As a model animal, Mongolian gerbils are often used, however, the genome of the inoculated H. Helicobacter pylori is a pathogenic bacterium that causes various gastrointestinal diseases in the human stomach.
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