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      Immune Response in Bacterial and Candida Sepsis

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          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.

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          Most cited references120

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          The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3).

          Definitions of sepsis and septic shock were last revised in 2001. Considerable advances have since been made into the pathobiology (changes in organ function, morphology, cell biology, biochemistry, immunology, and circulation), management, and epidemiology of sepsis, suggesting the need for reexamination.
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            A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17.

            Interleukin 17 (IL-17) has been linked to autoimmune diseases, although its regulation and function have remained unclear. Here we have evaluated in vitro and in vivo the requirements for the differentiation of naive CD4 T cells into effector T helper cells that produce IL-17. This process required the costimulatory molecules CD28 and ICOS but was independent of the cytokines and transcription factors required for T helper type 1 or type 2 differentiation. Furthermore, both IL-4 and interferon-gamma negatively regulated T helper cell production of IL-17 in the effector phase. In vivo, antibody to IL-17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused chemokine production and leukocyte infiltration. Thus, IL-17 expression characterizes a unique T helper lineage that regulates tissue inflammation.
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              The M1 and M2 paradigm of macrophage activation: time for reassessment

              Macrophages are endowed with a variety of receptors for lineage-determining growth factors, T helper (Th) cell cytokines, and B cell, host, and microbial products. In tissues, macrophages mature and are activated in a dynamic response to combinations of these stimuli to acquire specialized functional phenotypes. As for the lymphocyte system, a dichotomy has been proposed for macrophage activation: classic vs. alternative, also M1 and M2, respectively. In view of recent research about macrophage functions and the increasing number of immune-relevant ligands, a revision of the model is needed. Here, we assess how cytokines and pathogen signals influence their functional phenotypes and the evidence for M1 and M2 functions and revisit a paradigm initially based on the role of a restricted set of selected ligands in the immune response.
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                Author and article information

                Journal
                1886
                European Journal of Microbiology and Immunology
                EuJMI
                Akadémiai Kiadó
                2062-8633
                2019
                : 1-9
                Affiliations
                [1 ] Department of Intensive Care Medicine – Hospital Beatriz Ângelo, CEDOC, Nova Medical School , Portugal
                [2 ] Department of Emergency and Intensive Care Medicine - Centro Hospitalar Universitário São João , Faculdade de Medicina da Universidade do Porto, Grupo de Infeção e Sépsis, Portugal
                [3 ] Immunology Department, Nova Medical School and Immunoallergy Center, CUF Descobertas Hospital , Portugal
                Author notes
                [*]

                Author for correspondence: Tel.: 00351919474752; E-mail: patriciopatricia@ 123456gmail.com

                Article
                10.1556/1886.2019.00011
                dda5d1fd-8290-4edc-b3e0-523aa5d1ba5f
                © 2019 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License ( https://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited, a link to the CC License is provided, and changes - if any - are indicated.

                History
                : 29 May 2019
                : 19 August 2019
                Page count
                Pages: 9
                Categories
                Review Paper

                Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                PICS, Candida sepsis,cytokine storm,immune paralysis,immune response,ICU,sepsis,host immune response,CARS

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