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Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia

Excessive host inflammatory responses negatively impact disease outcomes in respiratory infection. Host-pathogen interactions during the infective phase of influenza are well studied, but little is known about the host’s response during the repair stage. Here, we show that influenza infection stimul...

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Autores principales: Li, Liang, Chong, Han Chung, Ng, Say Yong, Kwok, Ka Wai, Teo, Ziqiang, Tan, Eddie Han Pin, Choo, Chee Chong, Seet, Ju Ee, Choi, Hyung Won, Buist, Martin Lindsay, Chow, Vincent Tak Kwong, Tan, Nguan Soon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Authors. Published by Elsevier Inc. 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185373/
https://www.ncbi.nlm.nih.gov/pubmed/25660016
http://dx.doi.org/10.1016/j.celrep.2015.01.011
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author Li, Liang
Chong, Han Chung
Ng, Say Yong
Kwok, Ka Wai
Teo, Ziqiang
Tan, Eddie Han Pin
Choo, Chee Chong
Seet, Ju Ee
Choi, Hyung Won
Buist, Martin Lindsay
Chow, Vincent Tak Kwong
Tan, Nguan Soon
author_facet Li, Liang
Chong, Han Chung
Ng, Say Yong
Kwok, Ka Wai
Teo, Ziqiang
Tan, Eddie Han Pin
Choo, Chee Chong
Seet, Ju Ee
Choi, Hyung Won
Buist, Martin Lindsay
Chow, Vincent Tak Kwong
Tan, Nguan Soon
author_sort Li, Liang
collection PubMed
description Excessive host inflammatory responses negatively impact disease outcomes in respiratory infection. Host-pathogen interactions during the infective phase of influenza are well studied, but little is known about the host’s response during the repair stage. Here, we show that influenza infection stimulated the expression of angiopoietin-like 4 (ANGPTL4) via a direct IL6-STAT3-mediated mechanism. ANGPTL4 enhanced pulmonary tissue leakiness and exacerbated inflammation-induced lung damage. Treatment of infected mice with neutralizing anti-ANGPTL4 antibodies significantly accelerated lung recovery and improved lung tissue integrity. ANGPTL4-deficient mice also showed reduced lung damage and recovered faster from influenza infection when compared to their wild-type counterparts. Retrospective examination of human lung biopsy specimens from infection-induced pneumonia with tissue damage showed elevated expression of ANGPTL4 when compared to normal lung samples. These observations underscore the important role that ANGPTL4 plays in lung infection and damage and may facilitate future therapeutic strategies for the treatment of influenza pneumonia.
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spelling pubmed-71853732020-04-28 Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia Li, Liang Chong, Han Chung Ng, Say Yong Kwok, Ka Wai Teo, Ziqiang Tan, Eddie Han Pin Choo, Chee Chong Seet, Ju Ee Choi, Hyung Won Buist, Martin Lindsay Chow, Vincent Tak Kwong Tan, Nguan Soon Cell Rep Article Excessive host inflammatory responses negatively impact disease outcomes in respiratory infection. Host-pathogen interactions during the infective phase of influenza are well studied, but little is known about the host’s response during the repair stage. Here, we show that influenza infection stimulated the expression of angiopoietin-like 4 (ANGPTL4) via a direct IL6-STAT3-mediated mechanism. ANGPTL4 enhanced pulmonary tissue leakiness and exacerbated inflammation-induced lung damage. Treatment of infected mice with neutralizing anti-ANGPTL4 antibodies significantly accelerated lung recovery and improved lung tissue integrity. ANGPTL4-deficient mice also showed reduced lung damage and recovered faster from influenza infection when compared to their wild-type counterparts. Retrospective examination of human lung biopsy specimens from infection-induced pneumonia with tissue damage showed elevated expression of ANGPTL4 when compared to normal lung samples. These observations underscore the important role that ANGPTL4 plays in lung infection and damage and may facilitate future therapeutic strategies for the treatment of influenza pneumonia. The Authors. Published by Elsevier Inc. 2015-02-10 2015-02-05 /pmc/articles/PMC7185373/ /pubmed/25660016 http://dx.doi.org/10.1016/j.celrep.2015.01.011 Text en © 2015 The Authors Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.
spellingShingle Article
Li, Liang
Chong, Han Chung
Ng, Say Yong
Kwok, Ka Wai
Teo, Ziqiang
Tan, Eddie Han Pin
Choo, Chee Chong
Seet, Ju Ee
Choi, Hyung Won
Buist, Martin Lindsay
Chow, Vincent Tak Kwong
Tan, Nguan Soon
Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia
title Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia
title_full Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia
title_fullStr Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia
title_full_unstemmed Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia
title_short Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia
title_sort angiopoietin-like 4 increases pulmonary tissue leakiness and damage during influenza pneumonia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7185373/
https://www.ncbi.nlm.nih.gov/pubmed/25660016
http://dx.doi.org/10.1016/j.celrep.2015.01.011
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