Kogut Michael H, Arsenault Ryan J
USDA-ARS, SPARC, College Station, TX, USA.
Department of Animal and Food Sciences, University of Delaware, Newark, DE, USA.
Front Immunol. 2017 Apr 4;8:372. doi: 10.3389/fimmu.2017.00372. eCollection 2017.
The adaptation of to the eukaryotic host is a key process that enables the bacterium to survive in a hostile environment. have evolved an intimate relationship with its host that extends to their cellular and molecular levels. Colonization, invasion, and replication of the bacteria in an appropriate host suggest that modification of host functions is central to pathogenesis. Intuitively, this subversion of the cell must be a complex process, since hosts are not inherently programmed to provide an environment conducive to pathogens. Hosts have evolved countermeasures to pathogen invasion, establishment, and replication through two types of defenses: resistance and tolerance. Resistance functions to control pathogen invasion and reduce or eliminate the invading pathogen. Research has primarily concentrated on resistance mechanisms that are mediated by the immune system. On the other hand, tolerance is mediated by different mechanisms that limit the caused by a pathogen's growth without affecting or reducing pathogen numbers or loads. The mechanisms of tolerance appear to be separated into those that protect host tissues from the virulence factors of a pathogen and those that limit or reduce the damage caused by the host immune and inflammatory responses to the pathogen. Some pathogens, such as , have evolved the capacity to survive the initial robust immune response and persist. The persistent phase of a infection in the avian host usually involves a complex balance of protective immunity and immunopathology. is able to stay in the avian ceca for months without triggering clinical signs. Chronic colonization of the intestinal tract is an important aspect of persistent infection because it results in a silent propagation of bacteria in poultry stocks due to the impossibility to isolate contaminated animals. Data from our lab promote the hypothesis that have evolved a unique survival strategy in poultry that minimizes host defenses (disease resistance) during the initial infection and then exploits and/or induces a dramatic immunometabolic reprogramming in the cecum that alters the host defense to disease tolerance. Unfortunately, this disease tolerance results in the ongoing human food safety dilemma.
[细菌名称]对真核宿主的适应是一个关键过程,使该细菌能够在恶劣环境中生存。[细菌名称]与宿主进化出了一种深入到细胞和分子水平的密切关系。细菌在合适宿主中的定殖、侵袭和复制表明,宿主功能的改变是发病机制的核心。直观地说,这种对细胞的颠覆必定是一个复杂的过程,因为宿主并非天生就被设定要提供有利于病原体的环境。宿主通过两种防御方式进化出了应对病原体侵袭、定殖和复制的对策:抗性和耐受性。抗性的作用是控制病原体的侵袭并减少或消除入侵的病原体。研究主要集中在由免疫系统介导的抗性机制上。另一方面,耐受性由不同机制介导,这些机制限制病原体生长所造成的[影响],而不影响或减少病原体数量或负荷。耐受性机制似乎可分为两类,一类保护宿主组织免受病原体毒力因子的影响,另一类限制或减少宿主对病原体的免疫和炎症反应所造成的损害。一些病原体,如[细菌名称],已经进化出在初始强烈免疫反应中存活并持续存在的能力。[细菌名称]在禽类宿主中的持续感染阶段通常涉及保护性免疫和免疫病理学的复杂平衡。[细菌名称]能够在禽类盲肠中停留数月而不引发临床症状。肠道的慢性定殖是[细菌名称]持续感染的一个重要方面,因为由于无法隔离受污染的动物,它导致细菌在禽群中无声传播。我们实验室的数据支持这样一种假说,即[细菌名称]在禽类中进化出了一种独特的生存策略,在初始感染期间将宿主防御(抗病性)降至最低,然后利用和/或诱导盲肠中显著的免疫代谢重编程,从而将宿主防御改变为疾病耐受性。不幸的是,这种疾病耐受性导致了持续存在的人类食品安全困境。