IL-6 ameliorates acute lung injury in influenza virus infection

Mei Lin Yang, Chung Teng Wang, Shiu Ju Yang, Chia Hsing Leu, Shun Hua Chen, Chao Liang Wu, Ai Li Shiau

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Interleukin 6 (IL-6) is involved in innate and adaptive immune responses to defend against pathogens. It also participates in the process of influenza infection by affecting viral clearance and immune cell responses. However, whether IL-6 impacts lung repair in influenza pathogenesis remains unclear. Here, we studied the role of IL-6 in acute influenza infection in mice. IL-6-deficient mice infected with influenza virus exhibited higher lethality, lost more body weight and had higher fibroblast accumulation and lower extracellular matrix (ECM) turnover in the lung than their wild-type counterparts. Deficiency in IL-6 enhanced proliferation, migration and survival of lung fibroblasts, as well as increased virus-induced apoptosis of lung epithelial cells. IL-6-deficient lung fibroblasts produced elevated levels of TGF-β, which may contribute to their survival. Furthermore, macrophage recruitment to the lung and phagocytic activities of macrophages during influenza infection were reduced in IL-6-deficient mice. Collectively, our results indicate that IL-6 is crucial for lung repair after influenza-induced lung injury through reducing fibroblast accumulation, promoting epithelial cell survival, increasing macrophage recruitment to the lung and enhancing phagocytosis of viruses by macrophages. This study suggests that IL-6 may be exploited for lung repair during influenza infection.

Original languageEnglish
Article number43829
JournalScientific reports
Volume7
DOIs
Publication statusPublished - 2017 Mar 6

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Acute Lung Injury
Virus Diseases
Orthomyxoviridae
Interleukin-6
Lung
Human Influenza
Fibroblasts
Macrophages
Infection
Epithelial Cells
Viruses
Lung Injury
Adaptive Immunity
Phagocytosis
Innate Immunity
Extracellular Matrix
Cell Survival
Body Weight
Apoptosis

All Science Journal Classification (ASJC) codes

  • General

Cite this

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title = "IL-6 ameliorates acute lung injury in influenza virus infection",
abstract = "Interleukin 6 (IL-6) is involved in innate and adaptive immune responses to defend against pathogens. It also participates in the process of influenza infection by affecting viral clearance and immune cell responses. However, whether IL-6 impacts lung repair in influenza pathogenesis remains unclear. Here, we studied the role of IL-6 in acute influenza infection in mice. IL-6-deficient mice infected with influenza virus exhibited higher lethality, lost more body weight and had higher fibroblast accumulation and lower extracellular matrix (ECM) turnover in the lung than their wild-type counterparts. Deficiency in IL-6 enhanced proliferation, migration and survival of lung fibroblasts, as well as increased virus-induced apoptosis of lung epithelial cells. IL-6-deficient lung fibroblasts produced elevated levels of TGF-β, which may contribute to their survival. Furthermore, macrophage recruitment to the lung and phagocytic activities of macrophages during influenza infection were reduced in IL-6-deficient mice. Collectively, our results indicate that IL-6 is crucial for lung repair after influenza-induced lung injury through reducing fibroblast accumulation, promoting epithelial cell survival, increasing macrophage recruitment to the lung and enhancing phagocytosis of viruses by macrophages. This study suggests that IL-6 may be exploited for lung repair during influenza infection.",
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IL-6 ameliorates acute lung injury in influenza virus infection. / Yang, Mei Lin; Wang, Chung Teng; Yang, Shiu Ju; Leu, Chia Hsing; Chen, Shun Hua; Wu, Chao Liang; Shiau, Ai Li.

In: Scientific reports, Vol. 7, 43829, 06.03.2017.

Research output: Contribution to journalArticle

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