{"title":"Yersinia pestis and pneumonic plague: Insight into how a lethal pathogen interfaces with innate immune populations in the lung to cause severe disease","authors":"Gopinath Venugopal, Roger D. Pechous","doi":"10.1016/j.cellimm.2024.104856","DOIUrl":null,"url":null,"abstract":"<div><p><em>Yersinia pestis</em> is the causative agent of bubonic, septicemic and pneumonic plague. The historical importance and potential of plague to re-emerge as a threat worldwide are indisputable. The most severe manifestion of plague is pneumonic plague, which results in disease that is 100% lethal without treatment. <em>Y. pestis</em> suppresses host immune responses early in the lung to establish infection. The later stages of infection see the rapid onset of hyperinflammatory responses that prove lethal. The study of <em>Y. pestis</em> host/pathogen interactions have largely been investigated during bubonic plague and with attenuated strains in cell culture models. There remains a somewhat limited understanding of the interactions between virulent <em>Y. pestis</em> and immune populations in the lung that drive severe disease. In this review we give a broad overview of the progression of pneumonic plague and highlighting how <em>Y. pestis</em> interfaces with host innate immune populations in the lung to cause lethal disease.</p></div>","PeriodicalId":9795,"journal":{"name":"Cellular immunology","volume":"403 ","pages":"Article 104856"},"PeriodicalIF":3.7000,"publicationDate":"2024-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cellular immunology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0008874924000595","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Yersinia pestis is the causative agent of bubonic, septicemic and pneumonic plague. The historical importance and potential of plague to re-emerge as a threat worldwide are indisputable. The most severe manifestion of plague is pneumonic plague, which results in disease that is 100% lethal without treatment. Y. pestis suppresses host immune responses early in the lung to establish infection. The later stages of infection see the rapid onset of hyperinflammatory responses that prove lethal. The study of Y. pestis host/pathogen interactions have largely been investigated during bubonic plague and with attenuated strains in cell culture models. There remains a somewhat limited understanding of the interactions between virulent Y. pestis and immune populations in the lung that drive severe disease. In this review we give a broad overview of the progression of pneumonic plague and highlighting how Y. pestis interfaces with host innate immune populations in the lung to cause lethal disease.
鼠疫耶尔森菌是鼠疫、败血症和肺鼠疫的病原体。鼠疫在历史上的重要性和重新成为全球威胁的可能性是毋庸置疑的。鼠疫最严重的表现是肺鼠疫,这种疾病不经治疗100%致命。鼠疫酵母菌在肺部早期会抑制宿主的免疫反应,从而形成感染。感染后期会迅速出现致命的高炎症反应。对鼠疫 Y. 的宿主/病原体相互作用的研究主要集中在鼠疫期间和细胞培养模型中的减毒菌株。目前,人们对剧毒鼠疫酵母菌与肺部免疫群体之间的相互作用的了解仍然有限。在这篇综述中,我们将概述肺鼠疫的发展过程,并重点介绍鼠疫酵母菌如何与肺部宿主先天性免疫种群相互作用,导致致命疾病。
期刊介绍:
Cellular Immunology publishes original investigations concerned with the immunological activities of cells in experimental or clinical situations. The scope of the journal encompasses the broad area of in vitro and in vivo studies of cellular immune responses. Purely clinical descriptive studies are not considered.
Research Areas include:
• Antigen receptor sites
• Autoimmunity
• Delayed-type hypersensitivity or cellular immunity
• Immunologic deficiency states and their reconstitution
• Immunologic surveillance and tumor immunity
• Immunomodulation
• Immunotherapy
• Lymphokines and cytokines
• Nonantibody immunity
• Parasite immunology
• Resistance to intracellular microbial and viral infection
• Thymus and lymphocyte immunobiology
• Transplantation immunology
• Tumor immunity.