Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection

The human respiratory syncytial virus (hRSV) remains one of the leading pathogens causing acute respiratory tract infections (ARTIs) in children younger than 2 years old, worldwide. Hospitalizations during the winter season due to hRSV-induced bronchiolitis and pneumonia increase every year. Despite...

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Main Authors: Karen Bohmwald, Nicolás M. S. Gálvez, Gisela Canedo-Marroquín, Magdalena S. Pizarro-Ortega, Catalina Andrade-Parra, Felipe Gómez-Santander, Alexis M. Kalergis
Format: Article
Language:English
Published: Frontiers Media S.A. 2019-03-01
Series:Frontiers in Immunology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fimmu.2019.00452/full
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spelling doaj-38e45a58fb104abc9c2ec173a22307252020-11-25T00:35:16ZengFrontiers Media S.A.Frontiers in Immunology1664-32242019-03-011010.3389/fimmu.2019.00452426287Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus InfectionKaren Bohmwald0Nicolás M. S. Gálvez1Gisela Canedo-Marroquín2Magdalena S. Pizarro-Ortega3Catalina Andrade-Parra4Felipe Gómez-Santander5Alexis M. Kalergis6Alexis M. Kalergis7Millenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileMillenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileMillenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileMillenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileMillenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileMillenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileMillenium Institute on Immunology and Immunotherapy, Departamento de Genética Molecular y Microbiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, ChileDepartamento de Endocrinología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, ChileThe human respiratory syncytial virus (hRSV) remains one of the leading pathogens causing acute respiratory tract infections (ARTIs) in children younger than 2 years old, worldwide. Hospitalizations during the winter season due to hRSV-induced bronchiolitis and pneumonia increase every year. Despite this, there are no available vaccines to mitigate the health and economic burden caused by hRSV infection. The pathology caused by hRSV induces significant damage to the pulmonary epithelium, due to an excessive inflammatory response at the airways. Cytokines are considered essential players for the establishment and modulation of the immune and inflammatory responses, which can either be beneficial or harmful for the host. The deleterious effect observed upon hRSV infection is mainly due to tissue damage caused by immune cells recruited to the site of infection. This cellular recruitment takes place due to an altered profile of cytokines secreted by epithelial cells. As a result of inflammatory cell recruitment, the amounts of cytokines, such as IL-1, IL-6, IL-10, and CCL5 are further increased, while IL-10 and IFN-γ are decreased. However, additional studies are required to elicit the mediators directly associated with hRSV damage entirely. In addition to the detrimental induction of inflammatory mediators in the respiratory tract caused by hRSV, reports indicating alterations in the central nervous system (CNS) have been published. Indeed, elevated levels of IL-6, IL-8 (CXCL8), CCL2, and CCL4 have been reported in cerebrospinal fluid from patients with severe bronchiolitis and hRSV-associated encephalopathy. In this review article, we provide an in-depth analysis of the role of cytokines secreted upon hRSV infection and their potentially harmful contribution to tissue damage of the respiratory tract and the CNS.https://www.frontiersin.org/article/10.3389/fimmu.2019.00452/fullhuman respiratory syncytial viruscytokineschemokinestissue damageinflammation
collection DOAJ
language English
format Article
sources DOAJ
author Karen Bohmwald
Nicolás M. S. Gálvez
Gisela Canedo-Marroquín
Magdalena S. Pizarro-Ortega
Catalina Andrade-Parra
Felipe Gómez-Santander
Alexis M. Kalergis
Alexis M. Kalergis
spellingShingle Karen Bohmwald
Nicolás M. S. Gálvez
Gisela Canedo-Marroquín
Magdalena S. Pizarro-Ortega
Catalina Andrade-Parra
Felipe Gómez-Santander
Alexis M. Kalergis
Alexis M. Kalergis
Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection
Frontiers in Immunology
human respiratory syncytial virus
cytokines
chemokines
tissue damage
inflammation
author_facet Karen Bohmwald
Nicolás M. S. Gálvez
Gisela Canedo-Marroquín
Magdalena S. Pizarro-Ortega
Catalina Andrade-Parra
Felipe Gómez-Santander
Alexis M. Kalergis
Alexis M. Kalergis
author_sort Karen Bohmwald
title Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection
title_short Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection
title_full Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection
title_fullStr Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection
title_full_unstemmed Contribution of Cytokines to Tissue Damage During Human Respiratory Syncytial Virus Infection
title_sort contribution of cytokines to tissue damage during human respiratory syncytial virus infection
publisher Frontiers Media S.A.
series Frontiers in Immunology
issn 1664-3224
publishDate 2019-03-01
description The human respiratory syncytial virus (hRSV) remains one of the leading pathogens causing acute respiratory tract infections (ARTIs) in children younger than 2 years old, worldwide. Hospitalizations during the winter season due to hRSV-induced bronchiolitis and pneumonia increase every year. Despite this, there are no available vaccines to mitigate the health and economic burden caused by hRSV infection. The pathology caused by hRSV induces significant damage to the pulmonary epithelium, due to an excessive inflammatory response at the airways. Cytokines are considered essential players for the establishment and modulation of the immune and inflammatory responses, which can either be beneficial or harmful for the host. The deleterious effect observed upon hRSV infection is mainly due to tissue damage caused by immune cells recruited to the site of infection. This cellular recruitment takes place due to an altered profile of cytokines secreted by epithelial cells. As a result of inflammatory cell recruitment, the amounts of cytokines, such as IL-1, IL-6, IL-10, and CCL5 are further increased, while IL-10 and IFN-γ are decreased. However, additional studies are required to elicit the mediators directly associated with hRSV damage entirely. In addition to the detrimental induction of inflammatory mediators in the respiratory tract caused by hRSV, reports indicating alterations in the central nervous system (CNS) have been published. Indeed, elevated levels of IL-6, IL-8 (CXCL8), CCL2, and CCL4 have been reported in cerebrospinal fluid from patients with severe bronchiolitis and hRSV-associated encephalopathy. In this review article, we provide an in-depth analysis of the role of cytokines secreted upon hRSV infection and their potentially harmful contribution to tissue damage of the respiratory tract and the CNS.
topic human respiratory syncytial virus
cytokines
chemokines
tissue damage
inflammation
url https://www.frontiersin.org/article/10.3389/fimmu.2019.00452/full
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