Expression of three essential antioxidants of Helicobacter pylori in clinical isolates

Shi, Yanhong; Chen, Mo; Zhang, Yue-xia; Zhang, Jing; Ding, Shigang

doi:10.1631/jzus.b1300171

Cited by 11 publications

(9 citation statements)

References 24 publications

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“…Previously our data also revealed another two anti-oxidative factors, the arginase (RocF) and alkyl-hydroperoxide reductase (AhpC) levels were also higher in H. pylori isolated from gastric cancer patients [17]. RocF is also an important part of H. pylori redox system as Trx-1.…”

Section: Relationship Between Trx-1 and Other Antioxidant Memberssupporting

confidence: 54%

“…The RocF level was also higher in H. pylori isolated from cancer patients. What's more, our data showed a positive correlation trend between Trx-1 and AphC, although there was no linear trend, it might due to the limited sample number [17]. So we might come to the conclusion that it is the antioxidant enzyme system including Trx-1, RocF and AphC that contribute to the long term colonization of H. pylori in host stomach, and avoid H. pylori from oxidative damage.…”

Section: Relationship Between Trx-1 and Other Antioxidant Membersmentioning

confidence: 59%

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The Progress in Helicobacter Pylori High Risk Pathogenic Marke

Wang¹,

J²,

Shi³

et al. 2016

J Hepatol Gastroint Dis

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It has been widely accepted that Helicobacter pylori was closed related with tumorigenesis of gastric cancer, but the pathogenic factor of this bacteria as well as the intrinsic mechanism are still unclear. We analyzed the proteomics of Helicobacter pylori strains isolated from both gastritis and gastric cancer and discovered several differential proteins. Among these proteins the Thioredoxin-1 (Trx-1) was considered most significant. Trx-1 protein has an anti-oxidative function and might increase cellular proliferation and anti-apoptosis. It helped to protect Helicobacter pylori from the oxidative reaction from the host so as lead to the long term colonization. We carried out a series of researches on this protein. The results revealed that Trx-1 was highly expressed in Helicobacter pylori isolated from cancer patients compared with the bacteria from gastritis patients. In cell culture study, up-regulation of Trx-1 expression in GES-1 and BCG823 cell lines might increase cell growth and promote cells into S phase. What's more, infected with Helicobacter pylori that express high level Trx-1 might induced cell apoptosis, decreased the expression of cyclin D1 and upregulated p21 in GES-1 cell line, while increase cell proliferation, and upregulate cyclin D1 in BCG823 cell line, indicating an oncogenic effects. We further infected Mongolian gerbils by Helicobacter pylori with high level Trx-1. The results showed long term infection lead to serious pathologic change of the stomach mucosa and finally adenocarcinoma occurred. In conclusion, Helicobacter pylori Trx-1 may play an important role in the development of stomach adenocarcinoma and can be considered as pathogenic marker. Future studies are still necessary for the specific process of Trx-1 protein on gastric mucosal after H. pylori infection, the relationship between clinical TNM stages and Hp Trx-1 level, as well as the downstream signal pathways that are involved in the carcinogenic process.

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Section: Relationship Between Trx-1 and Other Antioxidant Memberssupporting

confidence: 54%

Section: Relationship Between Trx-1 and Other Antioxidant Membersmentioning

confidence: 59%

The Progress in Helicobacter Pylori High Risk Pathogenic Marke

Wang¹,

J²,

Shi³

et al. 2016

J Hepatol Gastroint Dis

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“…DNA damage can be detected in the gastric mucosa during HP infection [ 17 , 28 ]. Our previous study found that the high-Trx1 HP was related to stronger cellular stress and redox activity-related proteins [ 29 , 30 ]. Consistent with the previous studies, we found that HP with high expression of Trx1 can produce much more 8-OHDG, suggesting that 8-OHDG may be one of the pathogenic mechanisms of HP Trx1.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori Thioredoxin1 May Play a Highly Pathogenic Role via the IL6/STAT3 Pathway

Yanlei

Ding

2022

Gastroenterology Research and Practice

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Background. Recent studies have shown that CagA is considered highly pathogenic to helicobacter pylori (HP) in Western populations. However, in East Asia, CagA positive HP can be up to 90%, but not all patients will lead to gastric cancer. Our research group has found that HP thioredoxin1 (Trx1) may be a marker of high pathogenicity. Here, we investigate whether HP Trx1 exerts high pathogenicity and its internal molecular mechanism. Materials and Methods. We constructed the coculture system of high-Trx1 HP and low-Trx1 HP strains with gastric epithelial cell lines separately and detected the influence of HP strains. The cells were stained by AM/PI, and the cell’s mortality was assessed by fluorescence microscope. The cell’s supernatants or precipitates were collected to detect the expression of IL6. In addition, the cell’s precipitates were collected, and the expression of p-STAT3 was detected by western blot. Furthermore, the cell’s supernatants were collected for detecting the expression of 8-OHDG to investigate the extent of DNA damage. Results. The high-Trx1 HP can cause higher mortality of GES-1 cells compared with the low-Trx1 HP group (high-Trx1 HP ( 4.53 ± 0.56 ) %, low-Trx1 HP ( 0.39 ± 0.10 ) %, P < 0.001 ). The mRNA and protein level of IL-6 in AGS and GES-1 cells were increased during HP infection, and the expression of IL-6 in the High-Trx1 HP group was much higher than the low-Trx1 HP group. Besides, the expression of p-STAT3 was higher in the HP-positive gastric mucosa. And the expression of p-STAT3 in the high-Trx1 HP group was significantly upregulated compared with the low-Trx1 HP group. Furthermore, the expression of 8-OHDG in the high-Trx1 group was much higher than the low-Trx1 group (high-Trx1 HP ( 5.47 ± 1.73 ) ng/ml, low-Trx1 HP ( 2.89 ± 1.72 ) ng/ml, P < 0.05 ). Conclusion. HP Trx1 may play as a marker of high pathogenicity, and the high-Trx1 HP could mediate the pathogenic process of HP infection via the IL6/STAT3 pathway.

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“…Conversely, some authors associate the presence of arginases, especially ARG2 , with the escape mechanisms of H. pylori , by causing a low availability of L-arginine and thus inhibiting the NOS2-dependent microbicidal activity. Moreover, the expression of arginase by H. pylori itself was associated with its carcinogenic activity [26]. We believe that the patients with chronic inactive gastritis established a mechanism of protection against infection, and with an increase in ARG1 , established a modulation process for regeneration.…”

Section: Discussionmentioning

confidence: 99%

Arginase-1 and Treg Profile Appear to Modulate Inflammatory Process in Patients with Chronic Gastritis: IL-33 May Be the Alarm Cytokine in H. pylori-Positive Patients

Silva

Rodrigues

et al. 2019

Mediators of Inflammation

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Helicobacter pylori (H. pylori) is a highly prevalent bacterium in our environment, directly involved in various upper digestive tract diseases, such as gastritis, peptic ulcer, and gastric cancer. Several molecules activating the immune system have been reported to be involved in containing H. pylori infection. This study is aimed at analyzing the mRNA expression of the cytokines IFN-γ, IL-17, IL-10, TGF-β, IL-6, IL-22, IL-23, and IL-33; transcription factors T-bet, RORC, and FOXP3; enzymes ARG1, ARG2, and NOS2; and neuropeptides VIP and TAC and their respective receptors VIPR1 and TACR1 in the stomach lining of patients with severe digestive disorders. One hundred and twenty six patients have been evaluated, presenting with symptoms in the upper digestive tract, with the clinical indication for an Upper Digestive Endoscopy exam. Two fragments of the mucosa of the gastric body and antrum have been collected for anatomopathological examination and to analyze the expression of enzymes, cytokines, and transcription factors using qPCR. Expression of the ARG1 gene was seen as significantly higher in the group of patients with chronic inactive gastritis than in the control group. Expression of the TGF-β gene and its FOXP3 transcription factor was significantly higher in the group of chronic inactive gastritis patients than in the control. Expression of IFN-γ, IL-17, IL-10, and TGF-β and the transcription factors, T-bet and RORC, in the presence or absence of H. pylori showed no significant difference. However, the expression of FOXP3 was significantly lower in H. pylori-positive patients than that in H. pylori-negative patients. ARG1 and Treg profile appeared to be modulating the inflammatory process, protecting patients from the tissue lesions with chronic inactive gastritis. Furthermore, we suggest that IL-33 may be a crucial mediator of the immune response against an infection, after gastric mucosal damage.

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Expression of three essential antioxidants of Helicobacter pylori in clinical isolates

Cited by 11 publications

References 24 publications

The Progress in Helicobacter Pylori High Risk Pathogenic Marke

The Progress in Helicobacter Pylori High Risk Pathogenic Marke

Helicobacter pylori Thioredoxin1 May Play a Highly Pathogenic Role via the IL6/STAT3 Pathway

Arginase-1 and Treg Profile Appear to Modulate Inflammatory Process in Patients with Chronic Gastritis: IL-33 May Be the Alarm Cytokine in H. pylori-Positive Patients

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