Targeting IL-1β and IL-17A Driven Inflammation during Influenza-Induced Exacerbations of Chronic Lung Inflammation

For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and...

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Vydáno v:	PloS one Ročník 9; číslo 6; s. e98440
Hlavní autoři:	Sichelstiel, Anke, Yadava, Koshika, Trompette, Aurélien, Salami, Olawale, Iwakura, Yoichiro, Nicod, Laurent P., Marsland, Benjamin J.
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Public Library of Science 11.06.2014 Public Library of Science (PLoS)
Témata:	Animals Antibodies, Neutralizing - immunology Antibodies, Neutralizing - therapeutic use Bacterial infections Biology Biology and Life Sciences Bronchitis Chronic Disease Chronic obstructive pulmonary disease Cytokines Emphysema Humans Infections Inflammation Influenza Influenza, Human - complications Influenza, Human - immunology Influenza, Human - therapy Interleukin Interleukin 1 Interleukin 1 Receptor Antagonist Protein - immunology Interleukin 1 Receptor Antagonist Protein - therapeutic use Interleukin-17 - antagonists & inhibitors Interleukin-17 - immunology Interleukin-1beta - antagonists & inhibitors Interleukin-1beta - immunology Leukocytes (neutrophilic) Lung diseases Medicine Medicine and Health Sciences Mice Mice, Inbred BALB C Mice, Inbred C57BL Neutrophil Infiltration Neutrophilia Neutrophils Obstructive lung disease Orthomyxoviridae Infections - complications Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - therapy Pneumonia - complications Pneumonia - immunology Pneumonia - therapy Pulmonary Disease, Chronic Obstructive - complications Pulmonary Disease, Chronic Obstructive - immunology Pulmonary Disease, Chronic Obstructive - therapy Recombinant Proteins - immunology Recombinant Proteins - therapeutic use Recruitment Rodents Therapeutic applications Viral infections Switzerland
ISSN:	1932-6203, 1932-6203
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Abstract	For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation.
AbstractList	For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation. For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation.For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation. For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation
Author	Trompette, Aurélien Salami, Olawale Nicod, Laurent P. Marsland, Benjamin J. Sichelstiel, Anke Iwakura, Yoichiro Yadava, Koshika
AuthorAffiliation	2 Molecular Biomedicine, ETHZ, Zurich, Switzerland Helmholtz Zentrum München/Ludwig-Maximilians-University Munich, Germany 1 Faculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland 3 Research Institute for Biomedical Sciences, Tokyo University of Science, Tokyo, Japan
AuthorAffiliation_xml	– name: 1 Faculty of Biology and Medicine, University of Lausanne, Service de Pneumologie, CHUV, Lausanne, Switzerland – name: 3 Research Institute for Biomedical Sciences, Tokyo University of Science, Tokyo, Japan – name: 2 Molecular Biomedicine, ETHZ, Zurich, Switzerland – name: Helmholtz Zentrum München/Ludwig-Maximilians-University Munich, Germany
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Copyright	2014 Sichelstiel et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2014 Sichelstiel et al 2014 Sichelstiel et al
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: AS BJM LN. Performed the experiments: AS KY AT OS. Analyzed the data: AS KY AT OS. Contributed reagents/materials/analysis tools: YI. Wrote the paper: AS BJM KY.
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Snippet	For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute...
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SubjectTerms	Animals Antibodies, Neutralizing - immunology Antibodies, Neutralizing - therapeutic use Bacterial infections Biology Biology and Life Sciences Bronchitis Chronic Disease Chronic obstructive pulmonary disease Cytokines Emphysema Humans Infections Inflammation Influenza Influenza, Human - complications Influenza, Human - immunology Influenza, Human - therapy Interleukin Interleukin 1 Interleukin 1 Receptor Antagonist Protein - immunology Interleukin 1 Receptor Antagonist Protein - therapeutic use Interleukin-17 - antagonists & inhibitors Interleukin-17 - immunology Interleukin-1beta - antagonists & inhibitors Interleukin-1beta - immunology Leukocytes (neutrophilic) Lung diseases Medicine Medicine and Health Sciences Mice Mice, Inbred BALB C Mice, Inbred C57BL Neutrophil Infiltration Neutrophilia Neutrophils Obstructive lung disease Orthomyxoviridae Infections - complications Orthomyxoviridae Infections - immunology Orthomyxoviridae Infections - therapy Pneumonia - complications Pneumonia - immunology Pneumonia - therapy Pulmonary Disease, Chronic Obstructive - complications Pulmonary Disease, Chronic Obstructive - immunology Pulmonary Disease, Chronic Obstructive - therapy Recombinant Proteins - immunology Recombinant Proteins - therapeutic use Recruitment Rodents Therapeutic applications Viral infections
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Title	Targeting IL-1β and IL-17A Driven Inflammation during Influenza-Induced Exacerbations of Chronic Lung Inflammation
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Volume	9
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