Helicobacter最新文献_第9页

Application of cefuroxime in the eradication therapy of Helicobacter pylori infection: A review article 头孢呋辛在根除幽门螺旋杆菌感染疗法中的应用：综述文章

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-04-11 DOI: 10.1111/hel.13073

Changmin Mi, Baojun Suo, Xueli Tian, Yuxin Wang, Lingling Ma, Zhiqiang Song

Background

Helicobacter pylori infection and its associated diseases represent a significant global health concern. Patients who cannot use amoxicillin pose a therapeutic challenge and necessitate alternative medications. Preliminary research indicates that cefuroxime demonstrates promising potential for eradicating H. pylori infection, and there is a lack of comprehensive review articles on the use of cefuroxime.

Materials and Methods

This study conducts a thorough systematic literature review and synthesis. A comprehensive systematic search was conducted in PubMed, Web of Science, EMBASE, China National Knowledge Infrastructure, China Biology Medicine disc, and Wanfang Data up to January 13, 2024. The search strategy utilized the following keywords: (Cefuroxime) AND (Helicobacter pylori OR Helicobacter nemestrinae OR Campylobacter pylori OR Campylobacter pylori subsp. pylori OR Campylobacter pyloridis OR H. pylori OR Hp) for both English and Chinese language publications. Sixteen studies from five different countries or regions were included in final literature review.

Results

Analysis results indicate that H. pylori is sensitive to cefuroxime, with resistance rates similar to amoxicillin being relatively low. Regimens containing cefuroxime have shown favorable eradication rates, which were comparable to those of the regimens containing amoxicillin. Regarding safety, the incidence of adverse reactions in cefuroxime-containing eradication regimens was comparable to that of amoxicillin-containing regimens or other bismuth quadruple regimens, with no significant increase in allergic reactions in penicillin-allergic patients. Regarding compliance, studies consistently report high compliance rates for regimens containing cefuroxime.

Conclusion

Cefuroxime can serve as an alternative to amoxicillin for the patients allergic to penicillin with satisfactory efficacies, safety, and compliance.

背景幽门螺旋杆菌感染及其相关疾病是全球关注的重大健康问题。不能使用阿莫西林的患者给治疗带来了挑战，需要使用替代药物。初步研究表明，头孢呋辛在根除幽门螺杆菌感染方面具有良好的潜力，但目前缺乏关于头孢呋辛使用情况的全面综述文章。材料与方法本研究进行了全面系统的文献综述。截至 2024 年 1 月 13 日，在 PubMed、Web of Science、EMBASE、中国国家知识基础设施、中国生物医学文献数据库和万方数据中进行了全面系统的检索。检索策略使用了以下关键词：（头孢呋辛）和（幽门螺旋杆菌或内膜螺旋杆菌或幽门弯曲杆菌或幽门弯曲杆菌亚种或幽门弯曲杆菌或幽门螺杆菌或Hp），同时检索英文和中文出版物。最终的文献综述包括来自五个不同国家或地区的 16 项研究。结果分析结果表明，幽门螺杆菌对头孢呋辛敏感，耐药率与阿莫西林相似，相对较低。含有头孢呋辛的治疗方案显示出良好的根除率，与含有阿莫西林的治疗方案相当。在安全性方面，含有头孢呋辛的根除方案的不良反应发生率与含有阿莫西林的方案或其他四联铋剂方案相当，青霉素过敏患者的过敏反应没有明显增加。在依从性方面，研究报告一致表明，含有头孢呋辛的治疗方案依从性较高。结论头孢呋辛可作为阿莫西林的替代品，用于对青霉素过敏的患者，其疗效、安全性和依从性均令人满意。

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引用次数: 0

Refractoriness to anti-Helicobacter pylori treatment attributed to phenotypic resistance patterns in patients with gastroduodenopathy in Guayaquil-Ecuador 瓜亚基尔-厄瓜多尔胃十二指肠病患者因表型耐药模式而对幽门螺杆菌抗生素治疗产生的耐药性

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-04-05 DOI: 10.1111/hel.13060

Javier David Lara Icaza, Rosalina Lara Tapia, Cástula Tania Castro Triana, Laura Catalina Romero Ramírez

Background

Treatment of Helicobacter pylori gastric infection is complex and associated with increased rates of therapeutic failure. This research aimed to characterize the H. pylori infection status, strain resistance to antimicrobial agents, and the predominant lesion pattern in the gastroduodenal mucosa of patients with clinical suspicion of refractoriness to first- and second-line treatment who were diagnosed and treated in a health center in Guayaquil, Ecuador.

Methods

A total of 374 patients with upper gastrointestinal symptoms and H. pylori infection were preselected and prescribed one of three triple therapy regimens for primary infection, as judged by the treating physician. Subsequently, 121 patients who returned to the follow-up visit with persistent symptoms after treatment were studied.

Results

All patients had H. pylori infection. Histopathological examination diagnosed chronic active gastritis in 91.7% of cases; premalignant lesions were observed in 15.8%. The three triple therapy schemes applied showed suboptimal efficacy (between 47.6% and 77.2%), with the best performance corresponding to the scheme consisting of a proton pump inhibitor + amoxicillin + levofloxacin. Bacterial strains showed very high phenotypic resistance to all five antimicrobials tested: clarithromycin, 82.9%; metronidazole, 69.7%; amoxicillin and levofloxacin, almost 50%; tetracycline, 38.2%. Concurrent resistance to clarithromycin–amoxicillin was 43.4%, to tetracycline–metronidazole 30.3%, to amoxicillin–levofloxacin 27.6%, and to clarithromycin–metronidazole 59.2%.

Conclusions

In vitro testing revealed resistance to all five antibiotics, indicating that H. pylori exhibited resistance phenotypes to these antibiotics. Consequently, the effectiveness of triple treatments may be compromised, and further studies are needed to assess refractoriness in quadruple and concomitant therapies.

背景幽门螺杆菌胃感染的治疗非常复杂，且治疗失败率较高。本研究旨在分析在厄瓜多尔瓜亚基尔市一家医疗中心接受诊断和治疗的幽门螺杆菌感染状况、菌株对抗菌药的耐药性以及临床怀疑对一线和二线治疗无效的患者胃十二指肠粘膜的主要病变模式。方法预选了374名有上消化道症状和幽门螺杆菌感染的患者，并根据主治医生的判断，为他们开出了治疗原发性感染的三种三联疗法中的一种。随后，研究了 121 名在治疗后因症状持续而复诊的患者。结果所有患者均感染了幽门螺杆菌。经组织病理学检查，91.7%的病例确诊为慢性活动性胃炎；15.8%的病例出现癌前病变。三种三联疗法的疗效均不理想（介于 47.6% 和 77.2% 之间），其中质子泵抑制剂+阿莫西林+左氧氟沙星的疗效最好。细菌菌株对测试的所有五种抗菌药都表现出极高的表型耐药性：克拉霉素，82.9%；甲硝唑，69.7%；阿莫西林和左氧氟沙星，近 50%；四环素，38.2%。同时对克拉霉素-阿莫西林产生耐药性的占 43.4%，对四环素-甲硝唑产生耐药性的占 30.3%，对阿莫西林-左氧氟沙星产生耐药性的占 27.6%，对克拉霉素-甲硝唑产生耐药性的占 59.2%。结论体外测试显示，幽门螺杆菌对所有五种抗生素都具有耐药性，表明幽门螺杆菌对这些抗生素具有耐药表型。因此，三联疗法的效果可能会受到影响，还需要进一步研究来评估四联疗法和并用疗法的耐药性。

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引用次数: 0

Helicobacter pylori enhances HLA-C expression in the human gastric adenocarcinoma cells AGS and can protect them from the cytotoxicity of natural killer cells 幽门螺杆菌能增强人类胃腺癌细胞 AGS 中 HLA-C 的表达，并能保护它们免受自然杀伤细胞的细胞毒性。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-22 DOI: 10.1111/hel.13069

Etikala Apoorva, Rini Jacob, Desirazu N. Rao, Santosh Kumar

Helicobacter pylori (H. pylori) seems to play causative roles in gastric cancers. H. pylori has also been detected in established gastric cancers. How the presence of H. pylori modulates immune response to the cancer is unclear. The cytotoxicity of natural killer (NK) cells, toward infected or malignant cells, is controlled by the repertoire of activating and inhibitory receptors expressed on their surface. Here, we studied H. pylori-induced changes in the expression of ligands, of activating and inhibitory receptors of NK cells, in the gastric adenocarcinoma AGS cells, and their impacts on NK cell responses. AGS cells lacked or had low surface expression of the class I major histocompatibility complex (MHC-I) molecules HLA-E and HLA-C—ligands of the major NK cell inhibitory receptors NKG2A and killer-cell Ig-like receptor (KIR), respectively. However, AGS cells had high surface expression of ligands of activating receptors DNAM-1 and CD2, and of the adhesion molecules LFA-1. Consistently, AGS cells were sensitive to killing by NK cells despite the expression of inhibitory KIR on NK cells. Furthermore, H. pylori enhanced HLA-C surface expression on AGS cells. H. pylori infection enhanced HLA-C protein synthesis, which could explain H. pylori-induced HLA-C surface expression. H. pylori infection enhanced HLA-C surface expression also in the hepatoma Huh7 and HepG2 cells. Furthermore, H. pylori-induced HLA-C surface expression on AGS cells promoted inhibition of NK cells by KIR, and thereby protected AGS cells from NK cell cytotoxicity. These results suggest that H. pylori enhances HLA-C expression in host cells and protects them from the cytotoxic attack of NK cells expressing HLA-C-specific inhibitory receptors.

幽门螺杆菌（H. pylori）似乎在胃癌中起着致病作用。在已确诊的胃癌中也发现了幽门螺杆菌。幽门螺杆菌的存在如何调节对癌症的免疫反应尚不清楚。自然杀伤（NK）细胞对感染细胞或恶性细胞的细胞毒性受其表面表达的激活和抑制受体谱系控制。在这里，我们研究了幽门螺杆菌诱导的胃腺癌 AGS 细胞中 NK 细胞激活和抑制受体配体表达的变化及其对 NK 细胞反应的影响。AGS 细胞表面缺乏或很少表达主要 NK 细胞抑制受体 NKG2A 和杀伤细胞 Ig 样受体（KIR）的 I 类主要组织相容性复合体（MHC-I）分子 HLA-E 和 HLA-C 配体。然而，AGS 细胞表面高表达激活受体 DNAM-1 和 CD2 的配体以及粘附分子 LFA-1。同样，尽管 NK 细胞表达抑制性 KIR，但 AGS 细胞对 NK 细胞的杀伤仍很敏感。此外，幽门螺杆菌增强了 AGS 细胞表面的 HLA-C 表达。幽门螺杆菌感染增强了HLA-C蛋白的合成，这可以解释幽门螺杆菌诱导的HLA-C表面表达。幽门螺杆菌感染也会增强肝癌 Huh7 和 HepG2 细胞的 HLA-C 表面表达。此外，幽门螺杆菌诱导的 AGS 细胞的 HLA-C 表面表达促进了 KIR 对 NK 细胞的抑制，从而保护 AGS 细胞免受 NK 细胞的细胞毒性。这些结果表明，幽门螺杆菌能增强宿主细胞中 HLA-C 的表达，保护它们免受表达 HLA-C 特异性抑制受体的 NK 细胞的细胞毒性攻击。

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引用次数: 0

Diagnosis by combination of endoscopic findings helps differentiate non-Helicobacter pylori Helicobacter-infected gastritis from Helicobacter pylori-infected gastritis 结合内镜检查结果进行诊断有助于区分非幽门螺旋杆菌感染性胃炎和幽门螺旋杆菌感染性胃炎。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-21 DOI: 10.1111/hel.13070

Takuma Okamura, Yugo Iwaya, Tadanobu Nagaya, Kazuki Horiuchi, Tatsuya Negishi, Hiroyoshi Ota, Takeji Umemura

Background

The characteristic endoscopic findings of non-Helicobacter pylori Helicobacter (NHPH) gastritis, including white marbled appearance and crack-like mucosa, have been reported. However, these findings can also manifest in H. pylori (HP)-infected gastritis. This study compared NHPH gastritis and mild atrophic HP gastritis to identify features that may enhance NHPH diagnosis.

Materials and Methods

A total of 2087 patients underwent upper gastrointestinal endoscopy and were histologically evaluated by multiple gastric mucosal biopsies according to the updated Sydney System (USS) at Shinshu University Hospital between 2005 and 2023. Among them, nine patients were classified into the NHPH group and 134 patients with HP infection and mild atrophy were classified into the HP group for retrospective comparisons of endoscopic findings and clinicopathological characteristics.

Results

All nine patients in the NHPH group (eight males [89%], median ± standard deviation [SD] age: 49 ± 13.0 years) were infected with H. suis. The 134 patients in the HP group contained 70 men (52%) and had a median ± SD age of 35 ± 19.9 years. Endoscopic findings were statistically comparable for white marbled appearance (three patients [33%] in the NHPH group and 37 patients [31%] in the HP group) and crack-like mucosa (three patients [33%] and 27 patients [20%], respectively). Diffuse redness was significantly less frequent in the NHPH group (one patient [14%] vs. 97 patients [72%], p < 0.001). White marbled appearance or crack-like mucosa without diffuse redness was significantly more common in the NHPH group (56% vs. 13%, p = 0.004), with a sensitivity and specificity of 56% and 87%, respectively. Mean USS neutrophil infiltration and Helicobacter density scores were significantly higher in the HP group (both p < 0.01), which might have influenced the endoscopic findings of diffuse redness.

Conclusions

When endoscopic findings of white marbled appearance or cracked-like mucosa are present, evaluation for diffuse redness may contribute to a more accurate diagnosis of NHPH gastritis.

背景：非幽门螺杆菌胃炎（NHPH）的特征性内镜检查结果，包括白色大理石样外观和裂纹状粘膜，已被报道过。然而，幽门螺杆菌（HP）感染性胃炎也会出现这些症状。本研究比较了NHPH胃炎和轻度萎缩性HP胃炎，以确定可增强NHPH诊断的特征：2005年至2023年间，共有2087名患者在信州大学医院接受了上消化道内镜检查，并根据最新的悉尼系统（USS）进行了多次胃黏膜活检的组织学评估。其中，9 名患者被归入 NHPH 组，134 名感染 HP 且轻度萎缩的患者被归入 HP 组，对内镜检查结果和临床病理特征进行回顾性比较：NHPH组的9名患者（8名男性[89%]，中位数±标准差[SD]年龄：49±13.0岁）均感染了猪链球菌。HP组的134名患者中有70名男性（52%），年龄中位数±标准差（SD）为35±19.9岁。内镜检查结果在白色大理石花纹外观（NHPH 组有 3 名患者[33%]，HP 组有 37 名患者[31%]）和裂纹状粘膜（分别有 3 名患者[33%]和 27 名患者[20%]）方面具有统计学可比性。弥漫性发红在 NHPH 组明显较少（1 名患者 [14%] 对 97 名患者 [72%]，P 结论）：当内镜检查发现粘膜出现白色大理石花纹或裂纹时，对弥漫性发红进行评估有助于更准确地诊断 NHPH 胃炎。

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引用次数: 0

Oral immunotherapy for Helicobacter pylori: Can it be trusted? A systematic review 幽门螺旋杆菌口服免疫疗法：可信吗？系统综述。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-21 DOI: 10.1111/hel.13067

Mohammad Hossein Peypar, Amin Vesal Yeganeh, Ali Ramazani, Arman Alizadeh, Mahdi Abdorrashidi, Amirmohammad Tohidinia, Mohammad Mahdi Shamlou, Mohammad Heiat

Background

Helicobacter pylori (H. pylori) is a rod-shaped, gram-negative, microaerophilic bacterium that can be identified by gram staining. Its relationship with cancer is significant since it is involved in approximately 80% of gastric cancers and 5.5% of all malignant cancers. Two lines of treatment have been defined for H. pylori, but almost 40% of patients do not respond to the first line. Recent trials have investigated oral Immunotherapy as a new treatment method. The aim of this systematic review was to investigate the potential effects of oral Immunotherapy on eradication rate of H. pylori in human studies.

Methods

The systematic review was performed according to PRISMA guidelines. We searched online databases, including Scopus, PubMed, and Web of Science (ISI). Our search strategy was limited to English articles and studies on human populations that use oral immunotherapy for H. pylori.

Results

The total number of primary research records in different databases was 2775. After removing duplicate articles (n = 870), we excluded 1829 for reasons including non-human studies, irrelevance to our study objective, non-English language, or lack of information. Of the remaining 76 articles, only seven had sufficient information, and the rest were excluded. The studies were divided into two groups: those that used bovine antibody and those that used immunoglobulin Y to eradicate H. pylori.

Conclusion

In the group of Immunoglobulin Y, three out of four studies suggest that using Immunoglobulin Y for the treatment of H. pylori infection is significant. However, the group using bovine antibody for the treatment of H. pylori infection has various results, as two out of three studies concluded that bovine antibody therapy is not significant.

背景：幽门螺杆菌（Helicobacter pylori，H. pylori）是一种杆状、革兰氏阴性、嗜微酵母菌，可通过革兰氏染色鉴定。幽门螺杆菌与癌症的关系非常密切，因为大约 80% 的胃癌和 5.5% 的恶性癌症都与幽门螺杆菌有关。幽门螺杆菌有两种治疗方法，但近 40% 的患者对第一种治疗方法无效。最近的试验将口服免疫疗法作为一种新的治疗方法进行了研究。本系统综述的目的是在人体研究中调查口服免疫疗法对幽门螺杆菌根除率的潜在影响：本系统综述根据 PRISMA 指南进行。我们搜索了在线数据库，包括 Scopus、PubMed 和 Web of Science (ISI)。我们的搜索策略仅限于使用口服免疫疗法治疗幽门螺杆菌的英文文章和关于人类的研究：不同数据库中的主要研究记录总数为 2775 条。去除重复文章（870 篇）后，我们排除了 1829 篇文章，原因包括非人类研究、与我们的研究目标不相关、非英语语言或缺乏信息。在剩余的 76 篇文章中，只有 7 篇提供了足够的信息，其余均被排除。这些研究被分为两组：使用牛抗体的研究和使用免疫球蛋白 Y 根除幽门螺杆菌的研究：结论：在免疫球蛋白 Y 组中，四项研究中有三项表明，使用免疫球蛋白 Y 治疗幽门螺杆菌感染效果显著。然而，使用牛抗体治疗幽门螺杆菌感染组的结果各不相同，三项研究中有两项认为牛抗体治疗效果不明显。

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引用次数: 0

Research progress in photodynamic therapy for Helicobacter pylori infection 幽门螺旋杆菌感染光动力疗法的研究进展。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-18 DOI: 10.1111/hel.13068

Qian Luo, Chunyan Liu, Aiping Zhang, Dekui Zhang

Helicobacter pylori (H. pylori) is a pathogenic microorganism that colonizes the human gastric mucosa and can lead to various gastric disorders, including gastritis, gastric ulcers, and gastric cancer. However, the increasing prevalence of antibiotic resistance in H. pylori has prompted the search for alternative treatment options. Photodynamic therapy has emerged as a potential alternative therapy, thus offering the advantage of avoiding some of the side effects associated with antibiotics and effectively targeting drug-resistant strains. In the postantibiotic era, photodynamic therapy (PDT) has shown promise as a novel treatment for H. pylori infection. This review focused on elucidating the mechanism of photodynamic therapy in the treatment of H. pylori. Additionally, we present an overview of the current research on photodynamic therapy by examining both standalone photodynamic therapy and combination therapies for H. pylori infection treatment. Furthermore, the safety profile of photodynamic therapy was also evaluated. Finally, we discuss the challenges and prospects associated with this innovative technology, with an aim to provide new insights and methodologies for the treatment of H. pylori infection.

幽门螺杆菌（Helicobacter pylori，H. pylori）是一种定植于人体胃黏膜的病原微生物，可导致各种胃部疾病，包括胃炎、胃溃疡和胃癌。然而，幽门螺杆菌的抗生素耐药性日益普遍，促使人们寻找替代治疗方案。光动力疗法作为一种潜在的替代疗法应运而生，它具有避免抗生素相关副作用和有效针对耐药菌株的优势。在后抗生素时代，光动力疗法（PDT）有望成为治疗幽门螺杆菌感染的一种新型疗法。本综述重点阐述了光动力疗法治疗幽门螺杆菌的机制。此外，我们还通过研究治疗幽门螺杆菌感染的独立光动力疗法和联合疗法，概述了目前有关光动力疗法的研究。此外，我们还评估了光动力疗法的安全性。最后，我们讨论了与这项创新技术相关的挑战和前景，旨在为治疗幽门螺杆菌感染提供新的见解和方法。

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引用次数: 0

Antagonizing roles of SHP1 in the pathogenesis of Helicobacter pylori infection SHP1 在幽门螺旋杆菌感染发病机制中的拮抗作用。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-12 DOI: 10.1111/hel.13066

Si Chen, Huilin Zhao, Yue Tian, Qianwen Wu, Jianhui Zhang, Shuzhen Liu, Ying Zhang, Yulong Wu, Boqing Li, Shu Chen, Zhiqiang Wang, Ruoyu Xiao, Xiaofei Ji

Background

SHP1 has been documented as a tumor suppressor and it was thought to play an antagonistic role in the pathogenesis of Helicobacter pylori infection. In this study, the exact mechanism of this antagonistic action was studied.

Materials and Methods

AGS, MGC803, and GES-1 cells were infected with H. pylori, intracellular distribution changes of SHP1 were first detected by immunofluorescence. SHP1 overexpression and knockdown were then constructed in these cells to investigate its antagonistic roles in H. pylori infection. Migration and invasion of infected cells were detected by transwell assay, secretion of IL-8 was examined via ELISA, the cells with hummingbird-like alteration were determined by microexamination, and activation of JAK2/STAT3, PI3K/Akt, and ERK pathways were detected by immunoblotting. Mice infection model was established and gastric pathological changes were evaluated. Finally, the SHP1 activator sorafenib was used to analyze the attenuating effect of SHP1 activation on H. pylori pathogenesis in vitro and in vivo.

Results

The sub-localization of SHP1 changed after H. pylori infection, specifically that the majority of the cytoplasmic SHP1 was transferred to the cell membrane. SHP1 inhibited H. pylori-induced activation of JAK2/STAT3 pathway, PI3K/Akt pathway, nuclear translocation of NF-κB, and then reduced EMT, migration, invasion, and IL-8 secretion. In addition, SHP1 inhibited the formation of CagA-SHP2 complex by dephosphorylating phosphorylated CagA, reduced ERK phosphorylation and the formation of CagA-dependent hummingbird-like cells. In the mice infection model, gastric pathological changes were observed and increased IL-8 secretion, indicators of cell proliferation and EMT progression were also detected. By activating SHP1 with sorafenib, a significant curative effect against H. pylori infection was obtained in vitro and in vivo.

Conclusions

SHP1 plays an antagonistic role in H. pylori pathogenesis by inhibiting JAK2/STAT3 and PI3K/Akt pathways, NF-κB nuclear translocation, and CagA phosphorylation, thereby reducing cell EMT, migration, invasion, IL-8 secretion, and hummingbird-like changes.

背景：SHP1是一种肿瘤抑制因子，被认为在幽门螺杆菌感染的发病机制中起着拮抗作用。本研究对这种拮抗作用的确切机制进行了研究：用幽门螺杆菌感染 AGS、MGC803 和 GES-1 细胞，首先用免疫荧光法检测 SHP1 在细胞内的分布变化。然后在这些细胞中构建 SHP1 的过表达和敲除，以研究其在幽门螺杆菌感染中的拮抗作用。通过Transwell试验检测感染细胞的迁移和侵袭，通过ELISA检测IL-8的分泌，通过显微镜检查确定蜂鸟样改变的细胞，通过免疫印迹检测JAK2/STAT3、PI3K/Akt和ERK通路的激活。建立小鼠感染模型并评估胃病理变化。最后，利用SHP1激活剂索拉非尼分析了SHP1激活对幽门螺杆菌体内外发病机制的抑制作用：结果：幽门螺杆菌感染后，SHP1的亚定位发生了变化，特别是大部分细胞质中的SHP1转移到了细胞膜上。SHP1可抑制幽门螺杆菌诱导的JAK2/STAT3通路、PI3K/Akt通路的激活和NF-κB的核转位，进而减少EMT、迁移、侵袭和IL-8的分泌。此外，SHP1 还能通过使磷酸化的 CagA 去磷酸化来抑制 CagA-SHP2 复合物的形成，减少 ERK 磷酸化和 CagA 依赖性蜂鸟样细胞的形成。在小鼠感染模型中，观察到胃部病理变化，IL-8 分泌增加，细胞增殖和 EMT 进展指标也被检测到。通过索拉非尼激活 SHP1，可在体外和体内对幽门螺杆菌感染产生显著疗效：结论：SHP1通过抑制JAK2/STAT3和PI3K/Akt通路、NF-κB核转位和CagA磷酸化，从而减少细胞的EMT、迁移、侵袭、IL-8分泌和蜂鸟样变化，在幽门螺杆菌发病机制中发挥拮抗作用。

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引用次数: 0

Impact of mixed-infection rate of clarithromycin-susceptible and clarithromycin-resistant Helicobacter pylori strains on the success rate of clarithromycin-based eradication treatment 对克拉霉素敏感和对克拉霉素耐药的幽门螺杆菌菌株混合感染率对克拉霉素根除治疗成功率的影响。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-08 DOI: 10.1111/hel.13062

Momoko Tsuda, Yoshiyuki Watanabe, Ritsuko Oikawa, Ryosuke Watanabe, Masayuki Higashino, Kimitoshi Kubo, Hiroyuki Yamamoto, Fumio Itoh, Mototsugu Kato

Background

Clarithromycin (CAM) resistance is a major contributor to the failure to eradicate Helicobacter pylori (H. pylori). The mixed-infection ratio of CAM-susceptible and CAM-resistant H. pylori strains differs among individuals. Pyrosequencing analysis can be used to quantify gene mutations at position each 2142 and 2143 of the H. pylori 23S rRNA gene in intragastric fluid samples. Herein, we aimed to clarify the impact of the rate of mixed infection with CAM-susceptible and CAM-resistant H. pylori strains on the success rate of CAM-containing eradication therapy.

Materials and Methods

Sixty-four H. pylori-positive participants who received CAM-based eradication therapy, also comprising vonoprazan and amoxicillin, were enrolled in this prospective cohort study. Biopsy and intragastric fluid samples were collected during esophagogastroduodenoscopy. H. pylori culture and CAM-susceptibility tests were performed on the biopsy samples, and real-time PCR and pyrosequencing analyses were performed on the intragastric fluid samples. The mutation rates and eradication success rates were compared.

Results

The overall CAM-based eradication success rate was 84% (54/64): 62% (13/21) for CAM-resistant strains, and 95% (39/41) for CAM-sensitive strains. When the mutation rate of the 23S rRNA gene was 20% or lower for both positions (2142 and 2143), the eradication success rate was 90% or more. However, when the mutation rate was 20% or higher, the eradication success rate was lower (60%).

Conclusions

The mutation rate of the CAM-resistance gene was related to the success of eradication therapy, as determined via pyrosequencing analysis.

背景：克拉霉素（CAM）耐药性是幽门螺旋杆菌（H. pylori）无法根除的主要原因。对克拉霉素（CAM）敏感的幽门螺杆菌菌株和对克拉霉素（CAM）耐药的幽门螺杆菌菌株的混合感染率因人而异。热测序分析可用于量化胃液样本中幽门螺杆菌 23S rRNA 基因第 2142 和 2143 位的基因突变。在此，我们旨在明确CAM易感和CAM耐药幽门螺杆菌菌株混合感染率对含CAM根除疗法成功率的影响：这项前瞻性队列研究共纳入了 64 名幽门螺杆菌阳性患者，他们都接受了以 CAM 为基础的根除疗法，其中还包括伏诺普拉赞和阿莫西林。在食管胃十二指肠镜检查过程中收集了活检样本和胃液样本。对活检样本进行了幽门螺杆菌培养和 CAM 药敏试验，对胃液样本进行了实时 PCR 和热序列分析。对突变率和根除成功率进行了比较：基于 CAM 的总体根除成功率为 84%（54/64）：对 CAM 耐药菌株的根除成功率为 62%（13/21），对 CAM 敏感菌株的根除成功率为 95%（39/41）。当 23S rRNA 基因在两个位置（2142 和 2143）的突变率均为 20% 或更低时，根除成功率为 90% 或更高。然而，当突变率为 20% 或更高时，根除成功率较低（60%）：结论：通过热测序分析确定，CAM抗性基因的突变率与根除治疗的成功率有关。

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引用次数: 0

Volatilomic signatures of different strains of Helicobacter pylori 不同幽门螺旋杆菌菌株的挥发性特征。

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-08 DOI: 10.1111/hel.13064

Reinis Vangravs, Linda Mežmale, Daria Ślefarska-Wolak, Edgars Dauss, Clemens Ager, Alejandro H. Corvalan, Elmer Andrés Fernández, Chris A. Mayhew, Marcis Leja, Paweł Mochalski

<div> <section> <h3> Background</h3> <p><i>Helicobacter pylori</i> (<i>H</i>. <i>pylori</i>) infection is the most extensively studied risk factor for gastric cancer. As with any bacteria, <i>H</i>. <i>pylori</i> will release distinctive odors that result from an emission of volatile metabolic byproducts in unique combinations and proportions. Effectively capturing and identifying these volatiles can pave the way for the development of innovative and non-invasive diagnostic methods for determining infection. Here we characterize the <i>H. pylori</i> volatilomic signature, pinpoint potential biomarkers of its presence, and evaluate the variability of volatilomic signatures between different <i>H. pylori</i> isolates.</p> </section> <section> <h3> Materials and Methods</h3> <p>Using needle trap extraction, volatiles in the headspace above <i>H. pylori</i> cultures were collected and, following thermal desorption at 290°C in a splitless mode, were analyzed using gas chromatography–mass spectrometry. The resulting volatilomic signatures of <i>H. pylori</i> cultures were compared to those obtained from an analysis of the volatiles in the headspace above the cultivating medium only.</p> </section> <section> <h3> Results</h3> <p>Amongst the volatiles detected, 21 showed consistent differences between the bacteria cultures and the cultivation medium, with 11 compounds being elevated and 10 showing decreased levels in the culture's headspace. The 11 elevated volatiles are four ketones (2-pentanone, 5-methyl-3-heptanone, 2-heptanone, and 2-nonanone), three alcohols (2-methyl-1-propanol, 3-methyl-1-butanol, and 1 butanol), one aromatic (styrene), one aldehyde (2-ethyl-hexanal), one hydrocarbon (n-octane), and one sulfur compound (dimethyl disulfide). The 10 volatiles with lower levels in the headspace of the cultures are four aldehydes (2-methylpropanal, benzaldehyde, 3-methylbutanal, and butanal), two heterocyclic compounds (2-ethylfuran and 2-pentylfuran), one ketone (2-butanone), one aromatic (benzene), one alcohol (2-butanol) and bromodichloromethane. Of the volatile species showing increased levels, the highest emissions are found to be for 3-methyl-1-butanol, 1-butanol and dimethyl disulfide. Qualitative variations in their emissions from the different isolates was observed.</p> </section> <section> <h3> Conclusions</h3> <p>The volatiles emitted by <i>H. pylori</i> provide a characteristic volatilome signature that has the potential of being developed as a tool for monitoring infections caused by this pathogen. Furthermore, using the volatilome signatur

背景：幽门螺杆菌（H. pylori）感染是研究最为广泛的胃癌风险因素。与其他细菌一样，幽门螺杆菌也会释放出独特的气味，这些气味是由独特组合和比例的挥发性代谢副产物释放出来的。有效捕捉和识别这些挥发性物质可以为开发创新的非侵入性诊断方法铺平道路，从而确定是否感染幽门螺杆菌。在这里，我们描述了幽门螺杆菌挥发物特征，指出了其存在的潜在生物标志物，并评估了不同幽门螺杆菌分离物之间挥发物特征的差异性：采用针阱萃取法收集幽门螺杆菌培养物顶层空间中的挥发性物质，并在 290°C 温度下以无分割模式进行热解吸后，使用气相色谱-质谱法进行分析。所得到的幽门螺杆菌培养物挥发物特征与仅对培养基上方顶空的挥发物进行分析所得到的特征进行了比较：结果：在检测到的挥发物中，有 21 种挥发物在细菌培养物和培养基之间表现出一致的差异，其中 11 种化合物在培养物顶层空间的含量升高，10 种化合物含量降低。这 11 种含量升高的挥发物包括 4 种酮（2-戊酮、5-甲基-3-庚酮、2-庚酮和 2-壬酮）、3 种醇（2-甲基-1-丙醇、3-甲基-1-丁醇和 1-丁醇）、1 种芳香族化合物（苯乙烯）、1 种醛（2-乙基-己醛）、1 种碳氢化合物（正辛烷）和 1 种硫化物（二甲基二硫）。培养物顶空中含量较低的 10 种挥发物是四种醛（2-甲基丙醛、苯甲醛、3-甲基丁醛和丁醛）、两种杂环化合物（2-乙基呋喃和 2-戊基呋喃）、一种酮（2-丁酮）、一种芳香族化合物（苯）、一种醇（2-丁醇）和溴二氯甲烷。在含量增加的挥发性物质中，3-甲基-1-丁醇、1-丁醇和二甲基二硫的排放量最高。不同分离物的挥发物排放量存在质的差异：结论：幽门螺杆菌释放的挥发性物质提供了一种特征性的挥发物特征，有可能被开发为监测由这种病原体引起的感染的工具。此外，利用挥发性特征，我们还能区分不同的幽门螺杆菌分离物。不过，这些挥发性物质也是识别胃癌挥发性标记物的潜在干扰因素。

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引用次数: 0

Disruption of the gastric epithelial barrier in Correa's cascade: Clinical evidence via confocal endomicroscopy 科雷亚级联征中胃上皮屏障的破坏：共聚焦内窥镜的临床证据

IF 4.4 2区医学 Q1 GASTROENTEROLOGY & HEPATOLOGY

Helicobacter

Pub Date : 2024-03-05 DOI: 10.1111/hel.13065

Shao-Tong Wang, Hua-Wei Yang, Wen-Lin Zhang, Zhen Li, Rui Ji

Background

Gastric epithelial barrier disruption constitutes a crucial step in gastric cancer (GC). We investigated these disruptions during the Correa's cascade timeline to correlate epithelial barrier dysfunction.

Materials and Methods

This study was conducted as a single-center, non-randomized clinical trial in China from May 2019 to October 2022. Patients with chronic atrophic gastritis (CAG), gastric intestinal metaplasia (GIM), low-grade intraepithelial neoplasia (LGIN), high-grade intraepithelial neoplasia (HGIN), and intramucosal carcinoma underwent probe-based confocal laser endomicroscopy (pCLE). The pCLE scoring system was used to assess gastric epithelial barrier disruption semi-quantitatively.

Results

We enrolled 95 patients who underwent a pCLE examination. The control group consisted of 15 individuals, and the experimental group included 17 patients with CAG, 27 patients with GIM, 20 patients with LGIN, and 16 patients with early gastric cancer (EGC). Apart from CAG, which showed no significant difference compared to the control group, a significantly higher incidence of gastric epithelial barrier damage was found in the GIM, LGIN, and EGC groups compared to the control group (Kruskal–Wallis H test = 69.295, p < 0.001). There is no difference in LGIN patients between GIM and LGIN areas, and there is no difference between the two groups compared with the EGC group. The intestinal metaplasia area in LGIN patients causes more severe gastric epithelial damage compared to that in non-LGIN patients. Additionally, compared to control group, a significant difference (p < 0.001) was noted between individuals with Helicobacter pylori-positive atrophic gastritis and those with IM, whereas no significant difference (p > 0.05) was observed among individuals with H. pylori-negative atrophic gastritis.

Conclusions

The gastric epithelial barrier remains dysfunctional from the initiation of H. pylori infection to GC progression. Beyond the “point of no return,” subsequent carcinogenesis processes may be attributed to other mechanisms.

背景：胃上皮屏障破坏是胃癌（GC）的关键步骤。我们研究了科雷亚级联时间线上的这些破坏，以关联上皮屏障功能障碍：本研究于2019年5月至2022年10月在中国进行了单中心、非随机临床试验。慢性萎缩性胃炎（CAG）、胃肠化生（GIM）、低级别上皮内瘤变（LGIN）、高级别上皮内瘤变（HGIN）和黏膜内癌患者接受了探针式共聚焦激光内镜（pCLE）检查。pCLE 评分系统用于半定量评估胃上皮屏障破坏情况：我们招募了 95 名接受 pCLE 检查的患者。对照组包括 15 人，实验组包括 17 名 CAG 患者、27 名 GIM 患者、20 名 LGIN 患者和 16 名早期胃癌（EGC）患者。除 CAG 与对照组相比无显著差异外，在幽门螺杆菌阴性的萎缩性胃炎患者中，GIM、LGIN 和 EGC 组的胃上皮屏障损伤发生率明显高于对照组（Kruskal-Wallis H 检验 = 69.295，P 0.05）：结论：从幽门螺杆菌感染开始到胃癌进展，胃上皮屏障一直处于功能失调状态。超过 "不归点 "后，随后的癌变过程可能归因于其他机制。

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引用次数: 0