The gastric bacterium Helicobacter pylori efficiently evades innate immune detection and persistently colonizes its human host. Understanding the genetic determinants that H. pylori uses to establish and maintain persistence, along with their cellular targets, is key to our understanding of the pathogenesis of this extraordinarily successful bacterial colonizer of the human stomach. This review highlights recent advances in elucidating innate immune recognition of H. pylori, its interactions with myeloid cells and the consequences that this very local infection has for immune responses at extragastric sites in models of allergy, autoimmunity and parasitic infection. The human-specific, gram-negative gastric colonizer and carcinogen H. pylori represents the prototype of a persistent bacterial pathogen. It is transmitted during early childhood, typically from mother to infant, and is believed to persist in its human host from the cradle to the grave. The tremendous success of H. pylori in infecting and colonizing half of the world's population, and in continuously accompanying humans since they migrated out of Africa over 60000 years ago, can largely be attributed to its ability to manipulate the host immune system to its own advantage, and to thereby ensure its own persistence and chronicity. In his final years as an active PI, Stanley Falkow increasingly recognized the need to understand bacterial persistence strategies as a prerequisite of understanding the pathogenesis of chronic bacterial infections, and, inspired in large part by Denise Monack's work on Salmonella persistence, many of our discussions at the time revolved around this topic. Multiple labs have since made important contributions to our understanding of innate immune detection of H. pylori, the types and polarization of adaptive immune responses that ensue, the ability of H. pylori to skew such immune responses to its advantage, and its ability to manipulate the host immune system with far-reaching, even systemic consequences. This review attempts to cover some of these topics, with a particular focus on the most recent contributions by researchers in the field.

中文翻译：

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胃病原体幽门螺杆菌的持久性，先天性免疫激活和免疫调节的机制。

胃细菌幽门螺杆菌可有效规避先天免疫检测并持续定居其人类宿主。了解幽门螺杆菌用来建立和维持持久性的遗传决定因素，以及它们的细胞靶点，是我们了解这种人类胃部非常成功的细菌定植器发病机理的关键。这篇综述突出了阐明幽门螺杆菌的固有免疫识别，其与髓样细胞的相互作用以及这种局部感染对过敏，自身免疫和寄生虫感染模型中胃外部位免疫反应的后果的最新进展。人类特异性，革兰氏阴性的胃菌落和致癌菌幽门螺杆菌代表了持久性细菌病原体的原型。它是在儿童早期传播的，通常从母亲到婴儿，并且据信可以从摇篮到坟墓一直存在于人类宿主中。幽门螺杆菌在感染和定居全球一半人口方面取得了巨大成功，并且自从人类60000多年前从非洲移出以来就不断陪伴人类，这在很大程度上可以归因于幽门螺杆菌利用自身优势操纵宿主免疫系统的能力，从而确保其自身的持久性和长期性。在成为活跃的PI的最后几年中，Stanley Falkow逐渐认识到需要了解细菌持久性策略，这是理解慢性细菌感染的发病机制的先决条件，并且在很大程度上受到Denise Monack关于沙门氏菌持久性的研究的启发，当时围绕这个话题。此后，多个实验室为我们对幽门螺杆菌的先天免疫检测，随之而来的适应性免疫反应的类型和极化，幽门螺杆菌将此类免疫反应偏向其优势的能力及其操纵能力的理解做出了重要贡献。宿主免疫系统具有深远甚至系统的后果。这篇综述试图涵盖其中一些主题，特别着重于该领域研究人员的最新贡献。