Crane Meredith J, Lee Kayla M, FitzGerald Ethan S, Jamieson Amanda M
Division of Biology and Medicine, Department of Molecular Microbiology and Immunology, Brown University, Providence, RI, United States.
Front Immunol. 2018 Jun 22;9:1421. doi: 10.3389/fimmu.2018.01421. eCollection 2018.
Much research on infectious diseases focuses on clearing the pathogen through the use of antimicrobial drugs, the immune response, or a combination of both. Rapid clearance of pathogens allows for a quick return to a healthy state and increased survival. Pathogen-targeted approaches to combating infection have inherent limitations, including their pathogen-specific nature, the potential for antimicrobial resistance, and poor vaccine efficacy, among others. Another way to survive an infection is to tolerate the alterations to homeostasis that occur during a disease state through a process called host tolerance or resilience, which is independent from pathogen burden. Alterations in homeostasis during infection are numerous and include tissue damage, increased inflammation, metabolic changes, temperature changes, and changes in respiration. Given its importance and sensitivity, the lung is a good system for understanding host tolerance to infectious disease. Pneumonia is the leading cause of death for children under five worldwide. One reason for this is because when the pulmonary system is altered dramatically it greatly impacts the overall health and survival of a patient. Targeting host pathways involved in maintenance of pulmonary host tolerance during infection could provide an alternative therapeutic avenue that may be broadly applicable across a variety of pathologies. In this review, we will summarize recent findings on tolerance to host lung infection. We will focus on the involvement of innate immune responses in tolerance and how an initial viral lung infection may alter tolerance mechanisms in leukocytic, epithelial, and endothelial compartments to a subsequent bacterial infection. By understanding tolerance mechanisms in the lung we can better address treatment options for deadly pulmonary infections.
许多关于传染病的研究都集中在通过使用抗菌药物、免疫反应或两者结合来清除病原体。病原体的快速清除有助于迅速恢复健康状态并提高生存率。针对病原体的抗感染方法存在固有的局限性,包括其病原体特异性、产生抗菌耐药性的可能性以及疫苗效力不佳等。在感染中存活的另一种方式是通过一种称为宿主耐受或恢复力的过程来耐受疾病状态下发生的内环境稳态改变,这一过程独立于病原体负荷。感染期间内环境稳态的改变多种多样,包括组织损伤、炎症增加、代谢变化、体温变化和呼吸变化。鉴于肺的重要性和敏感性,它是理解宿主对传染病耐受性的良好系统。肺炎是全球五岁以下儿童死亡的主要原因。其中一个原因是,当肺部系统发生巨大改变时,会极大地影响患者的整体健康和生存。针对感染期间维持肺部宿主耐受所涉及的宿主途径,可能提供一种可广泛应用于多种病理状况的替代治疗途径。在本综述中,我们将总结关于宿主肺部感染耐受性的最新研究发现。我们将重点关注固有免疫反应在耐受性中的作用,以及初始病毒性肺部感染如何改变白细胞、上皮细胞和内皮细胞区室对后续细菌感染的耐受机制。通过了解肺部的耐受机制,我们可以更好地应对致命肺部感染的治疗选择。