scholarly journals Monoclonal antibody against CXCL-10/IP-10 ameliorates influenza A (H1N1) virus induced acute lung injury

Cell Research ◽  
2013 ◽  
Vol 23 (4) ◽  
pp. 577-580 ◽  
Author(s):  
Wei Wang ◽  
Penghui Yang ◽  
Ying Zhong ◽  
Zhongpeng Zhao ◽  
Li Xing ◽  
...  
Cell Research ◽  
2011 ◽  
Vol 22 (3) ◽  
pp. 528-538 ◽  
Author(s):  
Chenggang Li ◽  
Penghui Yang ◽  
Yang Sun ◽  
Taisheng Li ◽  
Chen Wang ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e44110 ◽  
Author(s):  
Chenggang Li ◽  
Penghui Yang ◽  
Yanli Zhang ◽  
Yang Sun ◽  
Wei Wang ◽  
...  

2010 ◽  
Vol 49 (5) ◽  
pp. 427-430 ◽  
Author(s):  
Toshiki Yokoyama ◽  
Kenji Tsushima ◽  
Atsuhito Ushiki ◽  
Nobumitsu Kobayashi ◽  
Kazuhisa Urushihata ◽  
...  

Dose-Response ◽  
2021 ◽  
Vol 19 (2) ◽  
pp. 155932582110113
Author(s):  
Rufeng Lu ◽  
Yueguo Wu ◽  
Honggang Guo ◽  
Zhuoyi Zhang ◽  
Yuzhou He

Influenza A virus infections can cause acute lung injury (ALI) in humans; thus, the identification of potent antiviral agents is urgently required. Herein, the effects of salidroside on influenza A virus-induced ALI were investigated in a murine model. BALB/c mice were intranasally inoculated with H1N1 virus and treated with salidroside. The results of this study show that salidroside treatment (30 and 60 mg/kg) significantly attenuated the H1N1 virus-induced histological alterations in the lung and inhibited inflammatory cytokine production. Salidroside also decreased the wet/dry ratio, viral titers, and Toll-like receptor 4 expression in the lungs. Therefore, salidroside may represent a potential therapeutic reagent for the treatment of influenza A virus-induced ALI.


Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P114
Author(s):  
F Piza ◽  
F Carvalho ◽  
H Li ◽  
T Crochemore ◽  
R Rodrigues

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Lijuan Chen ◽  
Xin Yan ◽  
Qianlin Yan ◽  
Jiajun Fan ◽  
Hai Huang ◽  
...  

A new approach to treat infections of highly pathogenic influenza virus is to inhibit excessive innate immune response. JiuWei QiangHuo decoction has been used for centuries for the treatment of pulmonary disorders in China. In this study, we evaluated the anti-inflammatory activities of the modified JiuWei QiangHuo (MJWQH) decoction in the treatment of influenza A (H1N1) virus-induced severe pneumonia in mice. The results showed that MJWQH significantly increased the survival rate of H1N1-infected mice and suppressed the production of TNF-α, IL-1, IL-6, MCP-1, RANTES, and IFN-αon day 4 after infection. Moreover, oral administration of MJWQH efficiently inhibited virus replication and alleviated the severity of lung injuries. The results also showed that MJWQH may have potential therapeutic effect on severe lung injury induced by H1N1 virus by regulating the NF-κB pathway. Our study suggested that MJWQH might be an alternative therapy for the treatment of viral pneumonia.


2020 ◽  
Vol 20 (2) ◽  
pp. 33-44
Author(s):  
Andrei G. Aleksandrov ◽  
Tatiana N. Savateeva-Lyubimova ◽  
Kira I. Stosman ◽  
Arman A. Muzhikyan ◽  
Konstantin V. Sivak

Background. Acute lung injury is one of severe course of influenza infection with mortality up to 40% of patients, despite on etiological and pathogenetic therapy. The aim of the article to study of the effects of aminoguanidine on correcting on acute lung injury induced by influenza virus A/California/7/09MA (mouse-adapted) (H1N1)pdm09, collection Smorodintsev Research Institute of Influenza. Materials and methods. The study was performed on 95 outbred female mice. The mouse-adapted pandemic influenza virus A/California/7/09MA (H1N1)pdm09 was used for modeling viral infection at a dose of 1 LD50. The mortality was analysed. Levels of advanced glycation end-products (AGEs), proinflammatory cytokines in lung; saturation index and leukocytes marker parameters in blood; pathological and histological studies of lung were performed on 4 and 7 days post infection. Results. Aminoguanidine led to 2-fold decrease in mortality in mice with virus-induced acute lung injury; significantly suppressed the growth of AGEs and proinflammatory cytokine levels in lung; reduced decrease of saturation index and hematological inflammatory markers; decreased level of inflammatory injury in lung tissue. Conclusion. Aminoguanidine relieved virus-induced acute lung injury in mice. These AGEs inhibitor reduced the proinflammatory response and structural changes in respiratory tract epithelial cells induced by reactive carbonyl compounds on cell membrane.


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