Role of vacuolating cytotoxin A in Helicobacter pylori infection and its impact on gastric pathogenesis

causes, via the influence of several virulence factors, persistent infection of the stomach, which leads to severe complications. Vacuolating cytotoxin A (VacA) is observed in almost all clinical strains of H. pylori; however, only some strains produce the toxigenic and pathogenic VacA, which is influenced by the gene sequence variations. VacA exerts its action by causing cell vacuolation and apoptosis. We performed a PubMed search to review the latest literatures published in English language. Areas covered Articles regarding H. pylori VacA and its genotypes, architecture, internalization, and role in gastric infection and pathogenicity are reviewed. We included the search for recently published literature until January 2020. Expert opinion H. pylori VacA plays a crucial role in severe gastric pathogenicity. In addition, VacA mediated in vivo bacterial survival leads to persistent infection and an enhanced bacterial evasion from the action of antibiotics and the innate host defense system, which leads to drug evasion. VacA as a co-stimulator for the CagA phosphorylation may exert a synergistic effect playing an important role in the CagA-mediated pathogenicity

Editorial: The Role of Mobile Genetic Elements in Bacterial Evolution and Their Adaptability

info:eu-repo/semantics/publishedVersio

<原著>肝右葉切除における短肝静脈, 右肝静脈処理のための前方アプローチ

A simple procedure of right hepatic lobectomy for bulky liver tumors is proposed. The procedure is named "Anterior approach", which is characterized by transection of hepatic parenchyma without mobilization and rotation of the right hepatic lobe. The transection directly reaches the ventral surface of the retrohepatic inferior vena cava first at the portion of caudate process. The hepatic parenchymal transection proceeds from ventral to dorsal and from caudal to cranial. Several dorsal short hepatic veins are severed on the ventral surface of the IVC and the right hepatic vein is finally severed from inside. This method enables the minimization of operative stress and is especially useful for cases with a huge tumor in the right hepatic lobe which invades the diaphragm or thoraco-abdominal wall.巨大肝腫瘍に対する合理的な肝右葉切除法としての前方アプローチを紹介する. 肝右葉切除の標準手技として, 右葉の授動と脱転がある. これは肝の右側から, 肝部下大静脈に注ぐ短肝静脈や右肝静脈の剥離と切離を行う方法であるが, 後区域や右葉全体を占める巨大肝腫瘍の場合には, それらの手技は困難なことが多く, また腫瘍の破裂をきたす恐れもあり危険を伴う. 前方アプローチは, 右葉の脱転を行わずに直接肝実質を切離して, 肝部下大静脈腹側面に到達し, 尾状葉突起から頭側に向かつて肝実質の離断を進める方法である. 肝部下大静脈腹側面に注ぐ短肝静脈を, 順次肝離断面側から剥離処理し, 最後に右肝静脈の離断も同様に行う. 横隔膜浸潤, 胸壁, 腹壁浸潤がある場合には, 肝切離が終了してから合併切除として最後に行う. また本法は, 脱転による残存肝の阻血, 門脈血液鬱滞を回避出来る利点があり, 肝ミトコンドリアの酸化還元状態を反映する動脈血中ケトン体比(AKBR)の術中低下も軽微であることが判明しており, 手術侵襲の点からみても有用である前方アプローチの良い適応は, 1)後区域, 又は右葉全体を占拠するような巨大肝腫瘍の場合, 2)腫蕩が右横隔膜, 胸壁, 腹壁に浸潤している場合, 3)右葉の腫瘍の下大静脈への浸潤が疑われ, 下大静脈合併切除の要否を判定する場合, 4)肝障害のために右葉切除を行うには機能的予備力の点で不安がある場合, などである

Current understanding and management of Helicobacter pylori infection: an updated appraisal [version 1; referees: 3 approved]

In addition to its role in gastric conditions, Helicobacter pylori has been found to contribute to the development of several non-gastric issues in recent years. Eradication therapy is the only effective management strategy to minimize the H. pylori-related gastric cancer and extra-gastric complications. For an effective “test and treat” strategy, diagnosis and therapy are both important. Because the infection is usually asymptomatic, patient selection is a critical issue for timely diagnosis and many clinical and demographic factors should be considered. Clarithromycin and metronidazole resistance rates also need to be considered while eradication therapy is offered. In this report, we discuss the issues which must be taken into account for the correct and timely diagnosis and for the antibiotic therapy-based management of H. pylori infection

Systematic review and meta-analysis: the relationship between the Helicobacter pylori dupA gene and clinical outcomes

<p>Abstract</p> <p>Background</p> <p>In 2005, the first disease-specific <it>Helicobacter pylori </it>virulence factor that induced duodenal ulcer and had a suppressive action on gastric cancer has been identified, and was named duodenal ulcer promoting gene (<it>dupA</it>). However, the importance of the <it>dupA </it>gene on clinical outcomes is conflicting in subsequent studies. The aim of this study was to estimate the magnitude of the risk for clinical outcomes associated with <it>dupA </it>gene.</p> <p>Methods</p> <p>A meta-analysis of case-control studies which provided raw data on the infection rates with the <it>dupA</it>-positive <it>H. pylori </it>detected by polymerase chain reaction was performed.</p> <p>Results</p> <p>Seventeen studies with a total of 2,466 patients were identified in the search. Infection with the <it>dupA</it>-positive <it>H. pylori </it>increased the risk for duodenal ulcer by 1.41-fold (95% confidence interval [CI], 1.12-1.76) overall. Subgroup analysis showed that the summary odds ratio (OR) was 1.57 (95% CI, 1.19-2.06) in Asian countries and 1.09 (95% CI, 0.73-1.62) in Western countries. There was no association between the presence of the <it>dupA </it>gene and gastric cancer and gastric ulcer. Publication bias did not exist.</p> <p>Conclusion</p> <p>Our meta-analysis confirmed the importance of the presence of the <it>dupA </it>gene for duodenal ulcer, especially in Asian countries.</p

Helicobacter pylori vacuolating cytotoxin and gastric cancer risk: reconsidered

Although Helicobacter pylori (H. pylori) cause gastric cancer, cancer develops in a fraction of H. pylori infected patients. Based on the notion that polymorphisms in the H. pylori vacuolating cytotoxin gene might be a determinant of clinical outcome, Abdi et al. used meta-analysis to examine the association between vacA gene subtypes and the risk of developing atrophic gastritis, intestinal metaplasia or gastric cancer. H. pylori infection causes gastric mucosal inflammation which underlies the development of peptic ulcer disease and gastric cancer (2). The outcome of any H. pylori infection reflects complex interactions between the host, the bacterium and the environment. These interactions are evident clinically as marked geographic variation in the prevalence of H. pylori-related diseases