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Background: Although the association between Helicobacter pylori (H. pylori) infection and hepatic encephalopathy (HE) has been confirmed through some research, the results of these relevant studies still remain controversial. We conducted an updated meta-analysis based on published studies to address this issue., Methods: A systematic search was conducted, reviewing all studies about the association between H. pylori infection and HE, through November 2021. The outcome measures were presented as odds ratios (ORs) with 95% confidence intervals (CIs)., Results: In total, 13 studies provided data from 2784 subjects. H. pylori infection increased the risk of HE by 32% (OR = 2.32, 95% CI: 1.78-3.04). The effect became greater after hepatic encephalopathy was divided into overt HE and minimal hepatic encephalopathy (MHE) (HE OR = 2.66, 95% CI: 2.01-3.51, MHE OR = 1.74, 95% CI: 1.10-2.76). After H. pylori eradication, the risk of HE was reduced by 64%., Conclusions: H. pylori infection is significantly associated with HE, and the infection rate of H. pylori also increases with the severity of HE. Eradication of H. pylori has a protective effect on HE. Therefore, it is necessary to eradicate H. pylori in HE treatments., (© The Author(s) 2022. Published by Oxford University Press on behalf of Faculty of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Helicobacter pylori (H. pylori) may be a risk factor for hypertension, but the reported studies have given conflicting results. This study aimed to explore the association between H. pylori infection and hypertension risk and blood pressure., Method: PubMed, Embase, Web of Science, CNKI, Weipu, and Wanfang databases were searched for articles published up to June 2, 2021. Dual-selection and data abstraction were conducted. Random-effect models were used to measure pooled estimates. All data were analyzed with Stata 14.0 SE (StataCorp, College Station, TX, USA)., Results: A total of 55 studies with 198,750 individuals were included in the meta-analysis. Among them, 33 studies reported the relationship between H. pylori infection and the risk of hypertension, and 25 studies reported the association of H. pylori infection with systolic blood pressure (SBP) and diastolic blood pressure (DBP). Three studies reported both of the above. Meta-analysis showed that H. pylori infection increased the risk of hypertension by 32% (odd ratio: 1.32, 95% CI: 1.15-1.52). Compared with non-H. pylori-infection individuals, the subjects with H. pylori infection had elevated levels of SBP (WMD: 1.86, 95% CI: 1.21-2.50) and DBP (WMD: 1.12, 95% CI: 0.81-1.43)., Conclusion: This meta-analysis suggested that H. pylori infection increased the risk of hypertension. This may provide a new strategy for hypertension prevention. However, the association between H. pylori infection and hypertension needs to be confirmed in further prospective cohort studies., (© 2022 S. Karger AG, Basel.)

Background and Objectives: The role of α-enolase (ENO1) in Helicobacter pylori -related gastric lesions might be a critical factor in the pathogenesis, but remains undefined. Materials and Methods: This study investigated the differential expression of α-enolase in clinical gastric specimens and cultured normal/cancer cells in response to H. pylori ( cagA+ ) infection and cagA transfection using qPCR, Western blots and histochemical methods. Results: A total of 172 gastric specimens were collected from 142 patients, the former comprising chronic superficial gastritis (CSG), precancerous diseases (PCDs, including atrophic gastritis, intestinal metaplasia and dysplasia) and gastric cancer (GC) cases. Among the CSG and PCD cases, the H. pylori -infected group had significantly elevated ENO1 mRNA levels compared with the uninfected group. In the GC cases, differential ENO1 expressions were detected between the cancer tissues and the paracancerous tissues. Notably, significant difference was first detected between the GC cell (AGS) and the normal cell (GES-1) as a response of ENO1 to H. pylori infection and cagA transfection. Conclusions: This report reveals that ENO1 expression is associated with H. pylori infection, cagA transfection, co-culture duration, multiplicity of infection, gastric normal/cancerous cell lines and cellular differentiation. The findings may be crucial bases for further ascertaining H. pylori pathogenic mechanism and formulating novel therapeutic and diagnostic strategies.

Background: Helicobacter pylori (H pylori) infection may be a risk factor for cardiovascular disease (CVD), but the reported researches have given conflicting results., Aims: To investigate the association between H pylori infection and risk of atherosclerotic CVD., Materials and Methods: The studies were retrieved in Embase, PubMed, Web of Science (published from Jan 1, 1990, to Jan 31, 2020, language restrictions: English). All studies included used data from case-control studies and cohort studies of cardiovascular adverse events. Random effect models were used to measure pooled estimates. All data were analyzed with Stata 11.2 SE (StataCorp, College Station, TX)., Results: Helicobacter pylori infection increased the risk of adverse cardiovascular events by 51% (40 studies, n = 19 691, odd ratio [OR] = 1.51, 95% confidence interval [CI]: 1.34-1.70). The effect was greater for studies that the type of CVDs was myocardial infarction (MI) and cerebrovascular disease (MI OR = 1.80, 95% CI: 1.42-2.26, cerebrovascular disease OR = 1.54, 95% CI: 1.27-1.89). Meanwhile, CagA seropositive H pylori strains were associated with a significantly increased risk of cardiovascular adverse events based on published research data (OR = 1.73, 95% CI: 1.40-2.14)., Conclusion: In conclusion, H pylori infection enhanced the risk of atherosclerotic cardiovascular adverse events, especially in some patients with MI and cerebrovascular disease. This study will provide guidance for the targeted prevention and treatment of CVDs. But this association need to be confirmed by more prospective studies., (© 2020 John Wiley & Sons Ltd.)

Objective: To construct a food-grade bacterium producing and delivering H. pylori Lpp20 antigen and evaluate its immune efficacy against H. pylori challenges with aim to develop anti-H. pylori oral vaccines and functional foods., Results: Lpp20 was expressed as a 22 kDa protein in Lactococcus lactis, constituting 11.2% of the cell lysate proteins, and recognized by mouse antisera. Mice orally gavaged with the engineered bacterium had elevated serum IgG levels and lowered urease activity of stomach following H. pylori challenges., Conclusions: This study firstly reports a food-grade L. lactis strain delivering Lpp20 to mucosal immunization sites, demonstrating a novel efficient production and safe utilization mode of Lpp20, offering a promising vaccine candidate and health food sources.

Aim: To assess the effect of Lactobacillus supplementation on Helicobacter pylori eradication rates and side effects of the triple therapy., Methods: PubMed, Embase, Web of Science and Cochrane Library were searched for articles published up to July, 2019. Review Manager 5.3 and Stata 12.0 were used for statistical analyses., Results: The initial database search resulted in 852 articles. Through exclusion and screening, 11 randomized controlled trials involving a total of 724 patients were finally included in this meta-analysis. The H. pylori elimination rate in the Lactobacillus supplement group was significantly higher than that in the control group (RR 1.16, 95% CI 1.08-1.25, P<0.0001). Subgroup analysis showed that the eradication rates were significantly enhanced in both adults and children group, and no significant difference was detected between Asia and Europe group. In addition, sub-analysis based on duration of Lactobacillus supplementation showed the pooled RRs in the long-term and short-term groups were 1.17 (95%CI 1.06-1.30) and 1.16 (95% CI 1.04-1.30), respectively. Regarding the Lactobacillus strains, the pooled RR was 1.33 (95% CI 1.10-1.62) in the L. casei group, 1.18 (95% CI 1.03-1.34) in the L. reuteri group while 1.02 (95% CI 0.87-1.21) in the Lactobacillus GG group. As for the total side effects, Lactobacillus supplementation significantly reduced the incidence of taste disturbance (RR = 0.36, 95% CI 0.17-0.74, P = 0.005)., Conclusions: Lactobacillus supplementation during the treatment of Helicobacter pylori infection can effectively improve the eradication rates, and reduce the incidence of therapy-related taste disturbance., Competing Interests: The authors have declared that no competing interests exist.

Background and Objectives: To perform a systematic review and meta-analysis with the aim of determining the relationship between H. pylori infection and psoriasis. Methods : Pubmed, Embase, China National Knowledge Infrastructure (CNKI), and Web of Science were searched for articles published up to July, 2019. Review Manager 5.3 and Stata 12.0 were used for statistical analyses. Results : The initial database search resulted in 204 articles. Through exclusion and screening, 11 studies involving a total of 1741 participants were finally included in this meta-analysis. The odds ratio (OR) of H. pylori infection rate in the psoriasis group was significantly higher than that in the control group (OR = 1.19, 95% CI 1.15-2.52, P = 0.008). Subgroup analysis showed that no significant difference was detected between the Asia group and the Europe group. As for the methods of H. pylori detection, a statistically significant increase of H. pylori infection in the IgG ELISA test group was detected, compared with the urea breath test group. In addition, analysis based on the severity of psoriasis showed a statistically significant increase of H. pylori infection in moderate and severe psoriasis patients (OR = 2.27; 95% CI: 1.42-3.63, I 2 = 27%), but not in the mild psoriasis patients (OR = 1.10; 95% CI: 0.79-1.54, I 2 = 0%). Conclusion : H. pylori infection is associated with psoriasis, and psoriasis patients with H. pylori infection have higher Psoriasis Area and Severity Index (PASI) scores. The findings are of considerable significance for the clinical practices.

Current studies indicate that the anti- H. pylori protective efficacy of oral vaccines to a large extent depends on using mucosal adjuvants like E. coli heat-lable enterotoxin B unit (LtB). However, the mechanism by which Th17/Th1-driven cellular immunity kills H. pylori and the role of LtB remains unclear. Here, two L. lactis strains, expressing H. pylori NapA and LtB, respectively, were orally administrated to mice. As observed, the administration of LtB significantly enhanced the fecal SIgA level and decreased gastric H. pylori colonization, but also markedly aggravated gastric inflammatory injury. Both NapA group and NapA+LtB group had elevated splenocyte production of IL-8, IL-10, IL-12, IL-17, IL-23 and INF-γ. Notably, gastric leukocytes' migration or leakage into the mucus was observed more frequently in NapA+LtB group than in NapA group. This report is the first that discusses how LtB enhances vaccine-induced anti- H. pylori efficacy by aggravating gastric injury and leukocytes' movement into the mucus layer. Significantly, it brings up a novel explanation for the mechanism underlying mucosal cellular immunity destroying the non-invasive pathogens. More importantly, the findings suggest the necessity to further evaluate LtB's potential hazards to humans before extending its applications. Thus, this report can provide considerable impact on the fields of mucosal immunology and vaccinology.

Persistent infection with Helicobacter pylori confers an increased risk for the development of gastric cancer. In our previous investigations, we found that ENO1 was overexpression in cagA-positive H. pylori-infected gastric epithelial AGS cells by proteomic method, in contrast to the isogenic cagA knock out mutant H. pylori-infected cells. ENO1 is a newly identified oncoprotein overexpressed in some cancer. However, the relationship between H. pylori infection and ENO1 expression still remains undefined. The AGS gastric cancer cells were transfected with WT-cagA plasmid and PR-cagA plasmids. Expression of ENO1 mRNA and protein were measured by real-time quantitative PCR and western blot analysis. Signal protein inhibitor treatment was used to investigate the signal pathways. It was found that the ENO1 mRNA and protein overexpression levels were dependent on cagA gene expression and CagA protein phosphorylation. Further analysis revealed that the Src, MEK and ERK pathway was involved in this upregulation effect. Our data suggest that ENO1 was upregulated by CagA protein through activating the Src and MEK/ERK signal pathways, thereby providing a novel mechanism underlying H. pylori-mediated gastric diseases.

Helicobacter pylori is the principal cause of chronic active gastritis, peptic ulcer, and gastric cancer. To develop an oral vaccine against H. pylori infection, we had expressed the H. pylori ureB gene (Genbank accession no. FJ436980) in nisin-controlled expression vectors using Lactococcus lactis NZ3900 as host. The ureB gene was amplified by PCR from a H.pylori strain MEL-Hp27. Then the ureB gene was fused translationally downstream of the nisin-inducible promoter nisA in a L. lactis plasmid pNZ8149. Lactose utilization based on the complementation of the lacF gene was used as a dominant selection marker for the food-grade expression system employing L. lactis NZ3900. The conditions of UreB expression in this system were optimized by orthogonal experiment. The optimized conditions have been determined as follows: induction of expression was carried out at the cells density of OD(600) ≈ 0.4 with 25 ng/ml nisin, and harvest after 5 h. The maximum percentage of recombinant UreB was estimated to be 7% of total soluble cellular proteins and the yield was 12.9 μg/ml. Western blot demonstrated that the UreB protein was expressed in the L. lactis transformant and had favorable immunoreactivity. These results indicated that the lactococci-derived vaccines could be promising candidates as alternative vaccine strategies for preventing H. pylori infection.

In the development of an oral vaccine against Helicobacter pylori, H. pylori urease subunit B (UreB) was expressed in a food-grade delivery vehicle, Lactococcus lactis NZ3900. The ureB gene (Genbank accession no. FJ436980) was amplified by polymerase chain reaction (PCR) from MEL-Hp27. The PCR-amplified ureB gene was cloned in the E. coli-L. lactis shuttle vector pNZ8110 and transformed into E. coli MC1061. After the transformant had been identified, the recombinant plasmid was purified and electrotransformed into L. lactis NZ3900. The conditions of UreB expression in the L. lactis transformant were optimized by orthogonal experiment. The maltose binding protein (MBP)-UreB fusion protein expressed by TB(1)/pMAL-c2X-ureB was used to cultivate mice polyclonal anti-UreB serum after purification by the amylose prepacked column. The Western blot method was adopted to confirm whether the UreB expressed by L. lactis transformant had immunoreactivity. The optimized conditions for UreB expression were as follows. Nisin 40 ng/ml was added to the medium when the recombinant grew to OD(600) approximately 0.30-0.40 and the induction time lasted 5 h. As a result, the maximum yield of UreB was 27.26 microg/mL of medium, and the maximum percentage of UreB in cell extracts of the L. lactis transformant reached its peak at 20.19%. Western blot analysis showed that the UreB protein expressed by L. lactis transformant had favorable immunoreactivity. All these results make an appealing case for construction of the food-grade vaccine for H. pylori.