Patricia Patricio, José Artur Paiva, Luís Miguel Borrego
{"title":"Immune Response in Bacterial and <i>Candida</i> Sepsis.","authors":"Patricia Patricio, José Artur Paiva, Luís Miguel Borrego","doi":"10.1556/1886.2019.00011","DOIUrl":null,"url":null,"abstract":"<p><p>Sepsis leads to a systemic immune response, and despite the progress of modern medicine, it is still responsible for a high mortality rate. The immune response to sepsis is dependent on the innate and adaptive immune systems. The first line is the innate system, which requires complex and multiple pathways in order to eliminate the invading threats. The adaptive responses start after the innate response. The cell-mediated arm of CD4+ and CD8+ T and B cells is the main responsible for this response. A coordinated cytokine response is essential for the host immune response. A dysregulated response can lead to a hyperinflammatory condition (cytokine storm). This hyperinflammation leads to neutrophils activation and may also lead to organ dysfunction. An imbalance of this response can increase the anti-inflammatory response, leading to compensatory anti-inflammatory response syndrome (CARS), persistent inflammation-immunsupression, catabolism syndrome (PICS), and, above all, an immune paralysis stat. This immune paralysis leads to opportunistic infections, <i>Candida</i> species being one of the emerging microorganisms involved. The host immune response is different for bacterial or <i>Candida</i> sepsis. Immune responses for bacterial and <i>Candida</i> sepsis are described in this paper.</p>","PeriodicalId":11929,"journal":{"name":"European Journal of Microbiology & Immunology","volume":"9 4","pages":"105-113"},"PeriodicalIF":0.0000,"publicationDate":"2019-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/28/32/eujmi-09-105.PMC6945997.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Journal of Microbiology & Immunology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1556/1886.2019.00011","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2019/12/25 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Sepsis leads to a systemic immune response, and despite the progress of modern medicine, it is still responsible for a high mortality rate. The immune response to sepsis is dependent on the innate and adaptive immune systems. The first line is the innate system, which requires complex and multiple pathways in order to eliminate the invading threats. The adaptive responses start after the innate response. The cell-mediated arm of CD4+ and CD8+ T and B cells is the main responsible for this response. A coordinated cytokine response is essential for the host immune response. A dysregulated response can lead to a hyperinflammatory condition (cytokine storm). This hyperinflammation leads to neutrophils activation and may also lead to organ dysfunction. An imbalance of this response can increase the anti-inflammatory response, leading to compensatory anti-inflammatory response syndrome (CARS), persistent inflammation-immunsupression, catabolism syndrome (PICS), and, above all, an immune paralysis stat. This immune paralysis leads to opportunistic infections, Candida species being one of the emerging microorganisms involved. The host immune response is different for bacterial or Candida sepsis. Immune responses for bacterial and Candida sepsis are described in this paper.
败血症会导致全身性免疫反应,尽管现代医学在不断进步,但它仍然是导致高死亡率的罪魁祸首。败血症的免疫反应取决于先天性免疫系统和适应性免疫系统。第一道防线是先天性免疫系统,它需要复杂的多重途径才能消除入侵的威胁。适应性反应始于先天性反应之后。由 CD4+ 和 CD8+ T 细胞和 B 细胞组成的细胞介导臂是这种反应的主要负责人。协调的细胞因子反应对宿主免疫反应至关重要。反应失调会导致高炎症状态(细胞因子风暴)。这种过度炎症会导致中性粒细胞活化,还可能导致器官功能障碍。这种反应的失衡会增加抗炎反应,导致代偿性抗炎反应综合症(CARS)、持续性炎症-免疫抑制-分解代谢综合症(PICS),尤其是免疫瘫痪状态。这种免疫瘫痪会导致机会性感染,念珠菌就是其中一种新出现的微生物。细菌性败血症和念珠菌性败血症的宿主免疫反应是不同的。本文介绍了细菌性败血症和念珠菌性败血症的免疫反应。