Exploring virulence factors of Helicobacter pylori isolated from gastric biopsy

被引:1
作者
Javanbakhat, Parisa [1 ]
Peeridogaheh, Hadi [1 ,4 ]
Nemati, Rasool [3 ]
Yazdanbod, Abbas [3 ,4 ]
Teimourpour, Amir [5 ]
Sadeghnezhad, Mahin [1 ]
Esmaelizad, Majid [6 ]
Teimourpour, Roghayeh [1 ,2 ]
机构
[1] Ardabil Univ Med Sci, Sch Med, Dept Microbiol, Ardebil, Iran
[2] Ardabil Univ Med Sci, Zoonoses Res Ctr, Ardebil, Iran
[3] Ardabil Univ Med Sci, Sch Med, Dept Internal Med, Ardebil, Iran
[4] Ardabil Univ Med Sci, Digest Dis Res Ctr, Ardebil, Iran
[5] High Inst Res & Educ, Blood Transfus Res Ctr, Tehran, Iran
[6] Razi Vaccine & Serum Res Inst, Cent Lab, Karaj, Iran
关键词
H; pylori; Gastric biopsy; Peptic ulcer; Urease; Gastric cancer; GENES; VACA; ASSOCIATION; STRAINS; CAGA; PREVALENCE; RESISTANCE; DIVERSITY; RELEVANCE; GENOTYPES;
D O I
10.1007/s11033-023-09075-z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Background Helicobacter pylori (H. pylori) colonizes human gastric mucosa and is classified as class one carcinogenic bacteria. In this regard, this study aimed to detect major virulence factors in H. pylori strains recovered from gastric biopsy in patients referred to Aras Clinique in Ardabil, northwest of Iran (2019-2021). Materials and methods In this descriptive-cross sectional study, 287 dyspeptic patients were included. For bacterial isolation, gastric biopsy specimens (n=287) were taken from gastric antrum, then aseptically were cultured on the selective medium and incubated at 37C in microaerophilic conditions for 3-5 days. Results 25.18% of all (n = 70) patients were found to be infected with H. pylori upon endoscopy. Of them, 9 patients (12.857%) and 2 patients (2.875%) had peptic ulcer disease and gastric cancer respectively. According to the different patterns of virulence factors, 57 virutypes were identified in which oipA-vacAs1-vacAm2 (3, 4.28% n =) and oipA-vacAs1-vacAs2-vacAm2 (3, 4.28% n =) were the most common patterns. The simultaneous presence of vacAS2, vacAm2 and hopQ2 genes was observed in both patients with gastric cancer. OipA (n = 562.5%), VacAs1 (n = 6.75%), VacAs2 (n = 6.75%), and VacAm2 (n = 787.5%) were found to be the most prevalent virulence factor. Conclusion According previous studies, it is confirmed that the cagPAI gene cluster and vacA gene alleles are strongly correlated with gastritis and gastrointestinal tract adenocarcinomas. Our study indicated that 50% of the indigenous strains of H. pylori harbor these oncogenic genes and they are hypervirulent.
引用
收藏
页数:7
相关论文
共 46 条
[41]   Importance of Helicobacter pylori oipA in clinical presentation, gastric inflammation, and mucosal interleukin 8 production [J].
Yamaoka, Y ;
Kikuchi, S ;
El-Zimaity, HMT ;
Gutierrez, O ;
Osato, MS ;
Graham, DY .
GASTROENTEROLOGY, 2002, 123 (02) :414-424
[42]   Pathogenesis of Helicobacter pylori-Related Gastroduodenal Diseases from Molecular Epidemiological Studies [J].
Yamaoka, Yoshio .
GASTROENTEROLOGY RESEARCH AND PRACTICE, 2012, 2012
[43]   Clinical relevance of Helicobacter pylori sabA genotype in Japanese clinical isolates [J].
Yanai, Ayako ;
Maeda, Shin ;
Hikiba, Yoko ;
Shibata, Wataru ;
Ohmae, Tomoya ;
Hirata, Yoshihiro ;
Ogura, Keiji ;
Yoshida, Haruhiko ;
Omata, Masao .
JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, 2007, 22 (12) :2228-2232
[44]   A case of gastric and duodenal mucosa-associated lymphoid tissue lymphoma with multiple gastric cancers: a case report [J].
Yokoyama, Takashi ;
Tanaka, Tetsuya ;
Harada, Suzuka ;
Ueda, Takeshi ;
Ejiri, Goki ;
Sasaki, Shoh ;
Takeda, Maiko ;
Yoshimura, Atsushi .
SURGICAL CASE REPORTS, 2021, 7 (01)
[45]   Antibiotic Resistance of Helicobacter pylori in Iranian Children: A Systematic Review and Meta-Analysis [J].
Yousefi-Avarvand, Arshid ;
Vaez, Hamid ;
Tafaghodi, Mohsen ;
Sahebkar, Amir Hossein ;
Arzanlou, Mohsen ;
Khademi, Farzad .
MICROBIAL DRUG RESISTANCE, 2018, 24 (07) :980-986
[46]   Helicobacter pylori babA2, cagA, and s1 vacA genes work synergistically in causing intestinal metaplasia [J].
Zambon, CF ;
Navaglia, F ;
Basso, D ;
Rugge, M ;
Plebani, M .
JOURNAL OF CLINICAL PATHOLOGY, 2003, 56 (04) :287-291