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Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.

ABSTRACT: The H. pylori outer inflammatory protein A (OipA) is an outer membrane protein that contributes to gastric inflammation. OipA is believed to affect intra-cellular signalling and modulate the host signalling pathways. The aim of the current study was to clarify the role of OipA in H. pylori pathogenesis and its effect on host cell signalling pathways. To this end, the oipA gene was isolated and inserted into cloning and expression vectors. The recombinant plasmid was transferred into an expression host to produce OipA, which was subsequently purified by affinity chromatography and used for antibody production. A confluent monolayer of gastric cell lines was treated with various concentrations of OipA and investigated for attachment, toxicity, and apoptosis and alterations in signalling pathways. OipA bound to gastric cell lines confirming its role in the attachment of H. pylori to host cells. The ratio of Bax/Bcl-2 and caspase3, 8, FasL in the host cells were assessed and the results showed that the Bax/Bcl-2 ratio as well as the level of cleaved-caspase 3 was elevated in OipA-treated cells. These findings suggest that OipA can bind and induce toxic events as well as triggering apoptotic cascade in host gastric cells through intrinsic pathway.

SUBMITTER: Teymournejad O

PROVIDER: S-EPMC5556102 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature

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Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.

Teymournejad Omid O Mobarez Ashraf Mohabati AM Hassan Zuhair Mohammad ZM Talebi Bezmin Abadi Amin A

Scientific reports 20170814 1

The H. pylori outer inflammatory protein A (OipA) is an outer membrane protein that contributes to gastric inflammation. OipA is believed to affect intra-cellular signalling and modulate the host signalling pathways. The aim of the current study was to clarify the role of OipA in H. pylori pathogenesis and its effect on host cell signalling pathways. To this end, the oipA gene was isolated and inserted into cloning and expression vectors. The recombinant plasmid was transferred into an expressio ...[more]

PMID: 28808292

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Project description:Objective:The clinical outcomes of gastric diseases such as chronic gastritis, peptic ulcer, and gastric cancer have been attributed to the interplay of virulence factors of Helicobacter pylori (H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. Methods:Chronic gastritis, atrophic gastritis, and intestinal metaplasia specimens were obtained from patients who underwent endoscopy and surgical resection between January 2017 and December 2018; specimens from gastric cancer patients treated between January 2014 and December 2018 were also added. H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of cagA, vacA, iceA2, babA2, and oipA genes and their association with clinical outcomes. H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of. Results:H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of vacA, babA2, and oipA genes and their association with clinical outcomes. vacA, babA2, and oipA genes and their association with clinical outcomes. P=0.033, OR?=?2.64; 95% CI?=?1.44-4.82, P=0.033, OR?=?2.64; 95% CI?=?1.44-4.82, P=0.033, OR?=?2.64; 95% CI?=?1.44-4.82, H. pylori vacA +/babA2, and oipA genes and their association with clinical outcomes. P=0.033, OR?=?2.64; 95% CI?=?1.44-4.82. Conclusion:In this present study, we reported on the virulence genes of H. pylori infection to reveal their association with increased risk of chronic gastritis, precancerous gastric lesions, and gastric cancer. Precancerous gastric lesions with H. pylori vacA+/babA2+/oipA+ genotype increased the risk of gastric cancer.H. pylori), host genetic susceptibility, and host immune responses. This study investigated the presence of H. pylori vacA +/babA2, and oipA genes and their association with clinical outcomes.

Project description:Background: Helicobacter pylori is an important human pathogen that infects the human gastric mucosa leading to chronic inflammation which is responsible for severe gastroduodenal diseases. The Outer Inflammatory Protein A (OipA) of H. pylori is an important virulence factor. However, the role of OipA in gastric cancer and ulcer development is still not well-established. Phase variation within a CT dinucleotide repeat motif of oipA switches its expression “on” and “off”. This study aims to elucidate the role of OipA in H. pylori infection using oipA “on” and “off” clinical strains and oipA deletion mutant. Methods: Proteomics analysis was performed on AGS human gastric epithelial cell line post-infection with oipA “on” and “off” H. pylori using liquid chromatography / mass spectrometry (LC/MS). In addition, AGS apoptosis and cell cycle assays were performed. To confirm the findings, oipA deletion mutant (ΔoipA) was generated and expression of VacA was detected using Western blotting. Result: Expression of AGS proteins involve in human disease was suppressed / down-regulated post-infection with oipA “off” strains, as well as oipA mutant, compared to oipA “on” strains. Furthermore, oipA “off” strains and oipA mutant resulted in a higher level of apoptosis and G0/G1 cell-cycle arrest in AGS cells than oipA “on” strains. Interestingly, deletion of oipA was found to increase VacA production by the bacterium. Discussion: The capability of oipA “off” strains to induce apoptosis and suppress proteins having roles in human disease may suggest that these H. pylori may be less virulent or may even be protective against carcinogenesis compared to its oipA “on” counterparts. This may potentially explain the higher incidence of gastric cancer among East Asian which oipA “on” strains predominates. Conclusions: Data from this study strengthened our understanding of the role of H. pylori OipA as a virulence factor in chronic inflammation, metastasis and carcinogenesis.

Project description:BackgroundThere are geographic variations in the genotypes of Helicobacter pylori (H. pylori) cagA, vacA, iceA, oipA and dupA. The aim of the study was to investigate the distribution of these genotypes among H. pylori strains from five regions of China and their association with clinical outcomes.Materials and methodsGastric biopsy specimens were obtained from 348 patients with different gastrointestinal diseases in the five regions of China. The regional distribution was 89 patients from Shandong, 91 from Guangxi, 57 from Hunan, 58 from Qinghai and 53 from Heilongjiang. The presence of cagA, vacA, iceA, oipA and dupA genotypes was determined by polymerase chain reaction (PCR) from H. pylori DNA.ResultsA total of 269 H. pylori isolates were obtained, of which 74 isolates were from Shandong, 78 from Guangxi, 46 from Hunan, 33 from Qinghai and 38 from Heilongjiang. The cagA-positive status was predominant in the five regions. The predominant vacA genotypes were s1c (73.4%), m2 (70.6%) and i1 (92.9%). In strains from Shandong, s1a and m1 were dominant. By contrast, s1c was dominant in Guangxi and i1 was dominant in Hunan and Heilongjiang. The prevalence of m2 subtype in Qinghai (78.8%) was significantly higher than that in other regions (P < 0.05). The predominant iceA genotype was iceA1 and the frequency of iceA1 was significantly more prevalent in Hunan than in other regions (P < 0.05). The oipA status "on" gene was more frequent in Shandong (91.9%) and Guangxi (91%) than in Heilongjiang (71.7%) (P < 0.05). Conversely, the dupA-positive status was less than half in Shandong (31.1%) and Guangxi (15.4%), whereas it was 73.9% in Hunan and 81.8% in Qinghai (P < 0.001). There were no significant associations between the cagA, vacA, iceA, oipA genotypes and clinical outcomes. The dupA-positive strains were more common in peptic ulcer disease (PUD) patients than in non-ulcer dyspepsia (NUD) patients in Shandong and Guangxi (P < 0.05), but the association was not observed in other geographic regions.ConclusionsThere was significant geographic diversity of H. pylori genotypes in different regions of China and the presence of dupA gene can be considered as a marker for the development of gastroduodenal diseases. However, the cagA, iceA, vacA and oipA genes cannot be regarded for prediction of the clinical presentation of H. pylori infection in China.

Dataset Information

Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.

Publications

Binding of the Helicobacter pylori OipA causes apoptosis of host cells via modulation of Bax/Bcl-2 levels.

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