Department of Gastroenterology and Hepatology, University of Zurich, Zurich, Switzerland.
Second Medical Clinic, Faculty of Medicine, Ippokration Hospital, Aristotle University of Thessaloniki, Thessaloniki, Macedonia, Greece.
Ann N Y Acad Sci. 2020 Dec;1481(1):59-71. doi: 10.1111/nyas.14449. Epub 2020 Aug 7.
Since its discovery, Helicobacter pylori (H. pylori) has attracted attention in the biomedical world with its numerous pathophysiologic implications, both gastrointestinal and systemic. Beyond its well-established carcinogenic properties, emerging evidence also supports "harmful" proinflammatory and neurodegenerative roles of H. pylori. On the other hand, H. pylori infection has been proposed to be "protective" against several diseases, such as asthma and gastroesophageal reflux disease. Eosinophilic esophagitis (EoE) is a relatively new, allergen/immune-mediated disease, which has also been linked to these considerations. Main arguments are a postulated shift of immune responses by H. pylori from T helper 2 (T 2) to T 1 polarization, as well as a potential decline of the H. pylori burden with the dramatic parallel rise of ΕοΕ: a series of observational studies reported an inverse association. In this review, we counter these arguments by providing further epidemiological data, which point out that this generalization might be rather incomplete. We also discuss the limitations of the existing studies evaluating a possible association. Furthermore, we provide current evidence on common pathogenetic components, which share both entities. In summary, the claim that H. pylori is protective against EoE is rather incomplete, and further mechanistic studies are necessary to elucidate a possible association.
自发现以来，幽门螺杆菌（H. pylori）因其众多的胃肠和系统病理生理意义而在生物医学领域引起关注。除了已被证实的致癌特性外，新出现的证据还支持 H. pylori 具有“有害”的促炎和神经退行性作用。另一方面，H. pylori 感染被认为对多种疾病具有“保护”作用，例如哮喘和胃食管反流病。嗜酸粒细胞性食管炎（EoE）是一种相对较新的、过敏原/免疫介导的疾病，也与这些考虑因素有关。主要论点是 H. pylori 假设的免疫反应从辅助性 T 细胞 2（T 2）向 T 细胞 1 极化的转变，以及 H. pylori 负担的潜在下降与 EoE 的急剧平行上升之间的关系：一系列观察性研究报告了一种反比关系。在这篇综述中，我们通过提供进一步的流行病学数据来反驳这些论点，这些数据指出这种概括可能相当不完整。我们还讨论了评估可能关联的现有研究的局限性。此外，我们还提供了这两个实体共享的共同发病机制成分的当前证据。总之，H. pylori 对 EoE 具有保护作用的说法相当不完整，需要进一步的机制研究来阐明可能的关联。
