scholarly journals Impacts of allergic airway inflammation on lung pathology in a mouse model of influenza A virus infection

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0173008 ◽  
Author(s):  
Akira Kawaguchi ◽  
Tadaki Suzuki ◽  
Yuki Ohara ◽  
Kenta Takahashi ◽  
Yuko Sato ◽  
...  
2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Ahmed R. Alsuwaidi ◽  
Junu A. George ◽  
Saeeda Almarzooqi ◽  
Stacey M. Hartwig ◽  
Steven M. Varga ◽  
...  

2020 ◽  
Vol 8 (12) ◽  
pp. 1878
Author(s):  
Qingyu Wu ◽  
Ilka Jorde ◽  
Olivia Kershaw ◽  
Andreas Jeron ◽  
Dunja Bruder ◽  
...  

Allergic airway inflammation (AAI) involves T helper cell type 2 (Th2) and pro-inflammatory responses to aeroallergens and many predisposing factors remain elusive. Influenza A virus (IAV) is a major human pathogen that causes acute respiratory infections and induces specific immune responses essential for viral clearance and resolution of the infection. Beyond acute infection, IAV has been shown to persistently affect lung homeostasis and respiratory immunity. Here we asked how resolved IAV infection affects subsequently induced AAI. Mice infected with a sublethal dose of IAV were sensitized and challenged in an ovalbumin mediated mouse model for AAI after resolution of the acute viral infection. Histological changes, respiratory leukocytes, cytokines and airway hyperreactivity were analyzed in resolved IAV infection alone and in AAI with and without previous IAV infection. More than five weeks after infection, we detected persistent pneumonia with increased activated CD4+ and CD8+ lymphocytes as well as dendritic cells and MHCII expressing macrophages in the lung. Resolved IAV infection significantly affected subsequently induced AAI on different levels including morphological changes, respiratory leukocytes and lymphocytes as well as the pro-inflammatory cytokine responses, which was clearly diminished. We conclude that IAV has exceptional persisting effects on respiratory immunity with substantial consequences for subsequently induced AAI.


Cell Reports ◽  
2021 ◽  
Vol 35 (7) ◽  
pp. 109159
Author(s):  
Xiaoyuan Bai ◽  
Wenxian Yang ◽  
Xiaohan Luan ◽  
Huizi Li ◽  
Heqiao Li ◽  
...  

2007 ◽  
Vol 88 (10) ◽  
pp. 2627-2635 ◽  
Author(s):  
Alexey A. Matskevich ◽  
Karin Moelling

In mammals the interferon (IFN) system is a central innate antiviral defence mechanism, while the involvement of RNA interference (RNAi) in antiviral response against RNA viruses is uncertain. Here, we tested whether RNAi is involved in the antiviral response in mammalian cells. To investigate the role of RNAi in influenza A virus-infected cells in the absence of IFN, we used Vero cells that lack IFN-α and IFN-β genes. Our results demonstrate that knockdown of a key RNAi component, Dicer, led to a modest increase of virus production and accelerated apoptosis of influenza A virus-infected cells. These effects were much weaker in the presence of IFN. The results also show that in both Vero cells and the IFN-producing alveolar epithelial A549 cell line influenza A virus targets Dicer at mRNA and protein levels. Thus, RNAi is involved in antiviral response, and Dicer is important for protection against influenza A virus infection.


2012 ◽  
Vol 206 (4) ◽  
pp. 495-503 ◽  
Author(s):  
Jie Zhou ◽  
Kelvin Kai-Wang To ◽  
Hui Dong ◽  
Zhong-Shan Cheng ◽  
Candy Choi-Yi Lau ◽  
...  

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