Impact of Pepsin on Transcriptional Alteration ofHelicobacter pylori Virulence Genes
محل انتشار: بیست و سومین کنگره بین المللی میکروب شناسی ایران
سال انتشار: 1401
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 44
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شناسه ملی سند علمی:
MEDISM23_335
تاریخ نمایه سازی: 16 مهر 1401
چکیده مقاله:
Background and Aim : Helicobacter pylori could survive in the stomach and infect the epithelialcells. Its pathogenicity depends on the bacterial virulence factors that upon interaction with thehost are associated with histological changes, inflammatory response and carcinogenesis.Although it is known that acidity of the stomach could affect the pathogenicity of H. pylori, thereis a lack of data to indicate its interaction with gastric proteolytic enzymes. The current study aimsto shed light on the function of pepsin as the most important proteolytic enzyme of gastric tissuein the pathogenicity of H. pylori.Methods : Clinical isolates of H. pylori were provided using the culture method from the gastricbiopsies of patients subjected to endoscopy. A polymerase chain reaction was done to confirm theisolates and their virulence potential. Well-defined isolates with ureB+/flaA+/cagA+ genotypewere selected for in vitro transcriptional analysis. Accordingly, the selected isolates were treatedwith ۰.۵ and ۱ mg/mL pepsin for ۳۰ and ۹۰ min and relative changes in the transcription of ureB,flaA and cagA genes were measured using real-time PCR compared with the untreatedcounterparts.Results : Out of ۴۶ H. pylori isolates from ۱۶۸ biopsy samples, ۱۷ isolates with optimum growthin broth culture medium were screened for ureB, flaA and cagA genes. All the strains were ureBpositive, while ۹۴.۱% and ۸۲.۳% of them carried flaA and cagA genes, respectively.Transcriptional analysis showed down-regulation of ureB and flaA (Ranges between ۰.۲ to ۰.۰۰۸folds) and up-regulation of cagA (Ranges between ۳ and ۹ folds), while the strains sustained theirsurvival. No significant diversity in transcriptional levels was detected among the three testedstrains in response to different concentrations of pepsin.Conclusion : Results of our study showed induction of cagA and suppression of flaA and ureBtranscription in response to regular pepsin concentrations in the gastric juice. Further studies areneeded to show possible outcomes of this interplay on the H. pylori pathogenesis.
کلیدواژه ها:
نویسندگان
Amir Ebrahimi
Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
Ronak Bakhtiari
Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
Masoud Alebouyeh
Pediatric Infections Research Centre, Research Institute for Children’s Health, Shahid Beheshti University of Medical Sciences, Tehran, Iran