Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signaling

Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal r...

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Published ineLife Vol. 6
Main Authors Kedzierski, Lukasz, Tate, Michelle D, Hsu, Alan C, Kolesnik, Tatiana B, Linossi, Edmond M, Dagley, Laura, Dong, Zhaoguang, Freeman, Sarah, Infusini, Giuseppe, Starkey, Malcolm R, Bird, Nicola L, Chatfield, Simon M, Babon, Jeffrey J, Huntington, Nicholas, Belz, Gabrielle, Webb, Andrew, Wark, Peter Ab, Nicola, Nicos A, Xu, Jianqing, Kedzierska, Katherine, Hansbro, Philip M, Nicholson, Sandra E
Format Journal Article
LanguageEnglish
Published England eLife Sciences Publications Ltd 14.02.2017
eLife Sciences Publications, Ltd
Subjects
Animals
Body Weight
Cell Biology
Chronic obstructive pulmonary disease
COPD
Cytokines - secretion
Disease Models, Animal
EGFR
Epidermal growth factor
Epidermal growth factor receptors
Epithelial cells
Epithelium
Humans
Inflammation
influenza
Influenza A
Influenza A virus - immunology
innate immunity
Kinases
Mice
Mice, Knockout
Microbiology and Infectious Disease
Mortality
Orthomyxoviridae Infections - pathology
Orthomyxoviridae Infections - virology
PI3K
Receptor, Epidermal Growth Factor - antagonists & inhibitors
Respiratory tract
Signal Transduction
SOCS5
Suppressor of Cytokine Signaling Proteins - deficiency
Suppressor of Cytokine Signaling Proteins - metabolism
Viral infections
Viral Load
influenza
mouse
cell biology
PI3K
innate immunity
infectious disease
microbiology
human
virus
EGFR
COPD
SOCS5
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Abstract Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). -deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza.
AbstractList Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). -deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza.
Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). Socs5-deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. Socs5 levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza.
Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). Socs5-deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. Socs5 levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza. Influenza, commonly referred to as the flu, is a highly contagious disease caused by a virus. When an infected person coughs or sneezes, droplets containing the virus are released into the air. Other individuals nearby may breathe in the virus, which then enters the cells lining the lungs and multiplies. Some people are more susceptible to the influenza virus than others. In particular, individuals with chronic obstructive pulmonary disease (COPD) often suffer much worse flu symptoms and are more likely to be admitted to hospital. COPD results from smoke exposure, including cigarette smoke and, in developing countries, the smoke from cooking fires, but it is not clear why individuals with COPD are more susceptible to the influenza virus. The influenza virus gains entry to lung cells by manipulating receptors on the cell surface. A protein called SOCS5 is present inside these cells and has been suggested as a potential regulator of these receptors. Here, Kedzierski et al. reveal that SOCS5 plays a critical role in protecting lung cells in mice and humans from the virus. The experiments show that mice lacking the gene that encodes SOCS5 were more susceptible to infection by the influenza virus, had more severe symptoms of disease and increased amounts of virus in their lungs. Further experiments in lung cells collected from human volunteers show that SOCS5 levels increased in both healthy smokers and non-smokers in response to influenza infection. Conversely, SOCS5 levels in lung cells of smokers with COPD remained low after infection. This suggests that SOCS5 might be an important factor in the susceptibility of these patients to influenza. The next is step is to understand exactly how SOCS5 works, which may make it possible to develop new treatments that boost SOCS5 activity in influenza patients.
Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). Socs5-deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. Socs5 levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza.DOI: http://dx.doi.org/10.7554/eLife.20444.001
Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory conditions such as COPD, are particularly susceptible to influenza. Here we show that suppressor of cytokine signaling (SOCS) five has a pivotal role in restricting influenza A virus in the airway epithelium, through the regulation of epidermal growth factor receptor (EGFR). Socs5 -deficient mice exhibit heightened disease severity, with increased viral titres and weight loss. Socs5 levels were differentially regulated in response to distinct influenza viruses (H1N1, H3N2, H5N1 and H11N9) and were reduced in primary epithelial cells from COPD patients, again correlating with increased susceptibility to influenza. Importantly, restoration of SOCS5 levels restricted influenza virus infection, suggesting that manipulating SOCS5 expression and/or SOCS5 targets might be a novel therapeutic approach to influenza. DOI: http://dx.doi.org/10.7554/eLife.20444.001 Influenza, commonly referred to as the flu, is a highly contagious disease caused by a virus. When an infected person coughs or sneezes, droplets containing the virus are released into the air. Other individuals nearby may breathe in the virus, which then enters the cells lining the lungs and multiplies. Some people are more susceptible to the influenza virus than others. In particular, individuals with chronic obstructive pulmonary disease (COPD) often suffer much worse flu symptoms and are more likely to be admitted to hospital. COPD results from smoke exposure, including cigarette smoke and, in developing countries, the smoke from cooking fires, but it is not clear why individuals with COPD are more susceptible to the influenza virus. The influenza virus gains entry to lung cells by manipulating receptors on the cell surface. A protein called SOCS5 is present inside these cells and has been suggested as a potential regulator of these receptors. Here, Kedzierski et al. reveal that SOCS5 plays a critical role in protecting lung cells in mice and humans from the virus. The experiments show that mice lacking the gene that encodes SOCS5 were more susceptible to infection by the influenza virus, had more severe symptoms of disease and increased amounts of virus in their lungs. Further experiments in lung cells collected from human volunteers show that SOCS5 levels increased in both healthy smokers and non-smokers in response to influenza infection. Conversely, SOCS5 levels in lung cells of smokers with COPD remained low after infection. This suggests that SOCS5 might be an important factor in the susceptibility of these patients to influenza. The next is step is to understand exactly how SOCS5 works, which may make it possible to develop new treatments that boost SOCS5 activity in influenza patients. DOI: http://dx.doi.org/10.7554/eLife.20444.002
Author Infusini, Giuseppe
Wark, Peter Ab
Hansbro, Philip M
Chatfield, Simon M
Webb, Andrew
Linossi, Edmond M
Kedzierski, Lukasz
Tate, Michelle D
Hsu, Alan C
Nicholson, Sandra E
Freeman, Sarah
Huntington, Nicholas
Bird, Nicola L
Starkey, Malcolm R
Nicola, Nicos A
Kolesnik, Tatiana B
Dagley, Laura
Belz, Gabrielle
Babon, Jeffrey J
Kedzierska, Katherine
Xu, Jianqing
Dong, Zhaoguang
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/28195529$$D View this record in MEDLINE/PubMed
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ID FETCH-LOGICAL-c475t-9e47da032be5c44bf7f11ec588e30cdd2018bac098c3c1a3d5cfff478fd3d37c3
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ISSN 2050-084X
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Tue Sep 17 21:12:22 EDT 2024
Fri Oct 25 10:29:55 EDT 2024
Sat Nov 02 22:00:55 EDT 2024
Fri Dec 06 05:21:04 EST 2024
Wed Oct 16 00:59:56 EDT 2024
IsDoiOpenAccess true
IsOpenAccess true
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IsScholarly true
Keywords influenza
mouse
cell biology
PI3K
innate immunity
infectious disease
microbiology
human
virus
EGFR
COPD
SOCS5
Language English
License http://creativecommons.org/licenses/by/4.0
This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
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content type line 23
These authors contributed equally to this work.
These authors also contributed equally to this work.
ORCID 0000-0002-1314-2134
0000-0002-0587-5514
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Snippet Influenza virus infections have a significant impact on global human health. Individuals with suppressed immunity, or suffering from chronic inflammatory...
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SubjectTerms Animals
Body Weight
Cell Biology
Chronic obstructive pulmonary disease
COPD
Cytokines - secretion
Disease Models, Animal
EGFR
Epidermal growth factor
Epidermal growth factor receptors
Epithelial cells
Epithelium
Humans
Inflammation
influenza
Influenza A
Influenza A virus - immunology
innate immunity
Kinases
Mice
Mice, Knockout
Microbiology and Infectious Disease
Mortality
Orthomyxoviridae Infections - pathology
Orthomyxoviridae Infections - virology
PI3K
Receptor, Epidermal Growth Factor - antagonists & inhibitors
Respiratory tract
Signal Transduction
SOCS5
Suppressor of Cytokine Signaling Proteins - deficiency
Suppressor of Cytokine Signaling Proteins - metabolism
Viral infections
Viral Load
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Title Suppressor of cytokine signaling (SOCS)5 ameliorates influenza infection via inhibition of EGFR signaling
URI https://www.ncbi.nlm.nih.gov/pubmed/28195529
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Volume 6
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