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幽门螺杆菌可塑性区域基因与印度胃十二指肠疾病的表现相关。

Helicobacter pylori plasticity region genes are associated with the gastroduodenal diseases manifestation in India.

作者信息

Ganguly Mou, Sarkar Sagartirtha, Ghosh Prachetash, Sarkar Avijit, Alam Jawed, Karmakar Bipul Chandra, De Ronita, Saha Dhira Rani, Mukhopadhyay Asish K

机构信息

Division of Bacteriology, National Institute of Cholera and Enteric Diseases, P 33, CIT Road, Scheme XM, Beliaghata, Kolkata, 700010 India ; Department of Zoology, University of Calcutta, Kolkata, India.

Department of Zoology, University of Calcutta, Kolkata, India.

出版信息

Gut Pathog. 2016 Mar 22;8:10. doi: 10.1186/s13099-016-0093-5. eCollection 2016.

DOI:10.1186/s13099-016-0093-5
PMID:27006705
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4802902/
Abstract

BACKGROUND

Almost all Helicobacter pylori infected person develop gastritis and severe gastritis is supposed to be the denominator of peptic ulcer diseases, which may lead to gastric cancer. However, it is still an enigma why few strains are associated with ulcer formation, while others are not related with any disease outcome. Although a number of putative virulence factors have been reported for H. pylori, there are contradictory results regarding their connotation with diseases. Recently, there has been a significant attention in strain-specific genes outside the cag pathogenicity island, especially genes within plasticity regions. Studies demonstrated that certain genes in this region may play important roles in the pathogenesis of H. pylori-associated diseases. The aim of this study was to assess the role of selected genes (jhp0940, jhp0945, jhp0947 and jhp0949) in the plasticity region in relation to risk of H. pylori-related diseases in Indian population.

METHODS

A total of 113 H. pylori strains isolated from duodenal ulcer (DU) (n = 61) and non-ulcer dyspepsia (NUD) subjects (n = 52) were screened by PCR and Dot-Blot to determine the presence of these genes. The comparative study of IL-8 production and apoptosis were also done by co-culturing the AGS cells with H. pylori strains of different genotype.

RESULTS

PCR and Dot-Blot results indicated that the prevalence rates of jhp0940, jhp0945, jhp0947 and jhp0949 in the H. pylori strains were 9.8, 47.5, 50.8, 40.9 % and 17.3, 28.8, 26.9, 19.2 % isolated from DU and NUD, respectively. IL-8 production and apoptotic cell death were significantly higher in H. pylori strains containing jhp0945, jhp0947 and jhp0949 than the strains lacking those genes. Results indicated that the prevalence of jhp0945, jhp0947 and jhp0949 are associated with increased risk of severe diseases in India.

CONCLUSION

Our study showed that presence of jhp0945, jhp0947 and jhp0949 were significantly associated with symptomatic expressions along with the increased virulence during in vitro study whereas jhp0940 seems to be negatively associated with the disease. These results suggest that jhp0945, jhp0947 and jhp0949 could be useful prognostic markers for the development of duodenal ulcer in India.

摘要

背景

几乎所有感染幽门螺杆菌的人都会患上胃炎,而严重胃炎被认为是消化性溃疡疾病的基础,消化性溃疡疾病可能会导致胃癌。然而,为什么少数菌株会导致溃疡形成,而其他菌株与任何疾病结局都无关,这仍然是一个谜。尽管已经报道了许多假定的幽门螺杆菌毒力因子,但关于它们与疾病的关联存在相互矛盾的结果。最近,人们对cag致病岛以外的菌株特异性基因,特别是可塑性区域内的基因给予了极大关注。研究表明,该区域的某些基因可能在幽门螺杆菌相关疾病的发病机制中发挥重要作用。本研究的目的是评估可塑性区域中选定基因(jhp0940、jhp0945、jhp0947和jhp0949)在印度人群中与幽门螺杆菌相关疾病风险的关系。

方法

通过PCR和斑点印迹法对从十二指肠溃疡(DU)患者(n = 61)和非溃疡性消化不良(NUD)患者(n = 52)中分离出的总共113株幽门螺杆菌菌株进行筛选,以确定这些基因的存在情况。还通过将AGS细胞与不同基因型的幽门螺杆菌菌株共培养,对白细胞介素-8的产生和细胞凋亡进行了比较研究。

结果

PCR和斑点印迹结果表明,幽门螺杆菌菌株中jhp0940、jhp0945、jhp0947和jhp0949的流行率分别为9.8%、47.5%、50.8%、40.9%,从DU和NUD中分离出的菌株中这些基因的流行率分别为17.3%。含有jhp0945、jhp0947和jhp0949的幽门螺杆菌菌株中白细胞介素-8的产生和凋亡细胞死亡明显高于缺乏这些基因的菌株。结果表明,在印度,jhp0945、jhp0947和jhp0949的流行与严重疾病风险增加有关。

结论

我们的研究表明,在体外研究中,jhp0945、jhp0947和jhp0949的存在与症状表现以及毒力增加显著相关,而jhp0940似乎与疾病呈负相关。这些结果表明,jhp0945、jhp0947和jhp0949可能是印度十二指肠溃疡发生的有用预后标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/d78571dd977e/13099_2016_93_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/9ec9f626374f/13099_2016_93_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/bd6dba908445/13099_2016_93_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/fecbbd328bdb/13099_2016_93_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/10bdbf4051a8/13099_2016_93_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/4b18797d442b/13099_2016_93_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/3a4921d9952c/13099_2016_93_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/d78571dd977e/13099_2016_93_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/9ec9f626374f/13099_2016_93_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/bd6dba908445/13099_2016_93_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/fecbbd328bdb/13099_2016_93_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/10bdbf4051a8/13099_2016_93_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/4b18797d442b/13099_2016_93_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/3a4921d9952c/13099_2016_93_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c03c/4802902/d78571dd977e/13099_2016_93_Fig7_HTML.jpg

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