Polygonum chinense water decoction lessens acute lung injury in mice induced by influenza virus

2020 ◽  
Vol 16 (71) ◽  
pp. 600
Author(s):  
Xiuli Ji ◽  
Rongkui Liu ◽  
Zhao Zhang ◽  
Xueyang Peng ◽  
Yueling Su ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Polygonum Chinense

The active GLP-1 analogue liraglutide alleviates H9N2 influenza virus-induced acute lung injury in mice

2021 ◽  
Vol 150 ◽  
pp. 104645
Author(s):  
Yu Bai ◽  
Pengjing Lian ◽  
Jingyun Li ◽  
Zihui Zhang ◽  
Jian Qiao
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
H9n2 Influenza Virus

scholarly journals Carnosine markedly ameliorates H9N2 swine influenza virus-induced acute lung injury

2015 ◽  
Vol 96 (10) ◽  
pp. 2939-2950 ◽  
Author(s):  
Tong Xu ◽  
Cunlian Wang ◽  
Ruihua Zhang ◽  
Mingju Xu ◽  
Baojian Liu ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Swine Influenza Virus ◽  
Swine Influenza

The features of the course of virus-associated acute lung injury in mice with induced immunosuppression

2021 ◽  
Vol 21 (3) ◽  
pp. 75-80
Author(s):  
Andrey G. Aleksandrov
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Cytokines ◽  
Influenza Infection ◽  
Lung Damage ◽  
Experimental Therapy ◽  
Blood Oxygen ◽  
Blood Oxygen Saturation ◽  
Pro Inflammatory Cytokines

BACKGROUND: Among all groups of patients with virus-associated acute lung injury with influenza infection, the most severe course is observed in patients with immunosuppression. In this case, despite the studied mechanism of the course of combined pathology, the question of therapy in this group of patients remains unclear. AIM: To study the features of the course of acute lung injury in influenza infection with secondary immunosuppression in an experiment for the possibility of searching for experimental therapy for this combined pathology. MATERIALS AND METHODS: The study was performed on 115 outbred female mice. The mouse-adapted pandemic influenza virus A/California/7/09MA (H1N1)pdm09 was used for modeling viral acute lung injury. Experimental immunosuppression was reproduced by administration of methotrexate (1.25 mg/kg intraperitoneally, once every 3 days during 3 weeks before infection). During the experiment, mortality, blood oxygen saturation, the concentration of pro-inflammatory cytokines in the lungs, and the severity of lung injury were measured. RESULTS: The presence of experimental immunosuppression led to an exacerbation of acute lung injury in infected animals in terms of mortality and lung damage. Changes in the dynamics of proinflammatory cytokines (TNF-, IL-6, IL-1) in the lungs were observed during acute lung injury. Retarded recovery of the lungs functional activity was noted. CONCLUSIONS: The experimental immunosuppression contributed to the exacerbation of acute lung injury and to an increase in the duration of the pathology. These changes could be associated with an altered process of elimination of the pathogen. The reproduced model of combined pathology was used for searching a therapy for these complications.

scholarly journals Type I interferon limits influenza virus-induced acute lung injury by regulation of excessive inflammation in mice

2013 ◽  
Vol 99 (3) ◽  
pp. 230-237 ◽  
Author(s):  
Yojiro Arimori ◽  
Risa Nakamura ◽  
Hisakata Yamada ◽  
Kensuke Shibata ◽  
Naoyoshi Maeda ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Type I Interferon ◽  
Type I

C5a receptor1 inhibition alleviates influenza virus-induced acute lung injury

2018 ◽  
Vol 59 ◽  
pp. 12-20 ◽  
Author(s):  
Nianping Song ◽  
Pei Li ◽  
Yuting Jiang ◽  
Hong Sun ◽  
Jing Cui ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury

scholarly journals Influenza Virus Infection Induces Platelet-Endothelial Adhesion Which Contributes to Lung Injury

2015 ◽  
Vol 90 (4) ◽  
pp. 1812-1823 ◽  
Author(s):  
Michael G. Sugiyama ◽  
Asela Gamage ◽  
Roman Zyla ◽  
Susan M. Armstrong ◽  
Suzanne Advani ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Platelet Adhesion ◽  
Human Lung ◽  
Influenza Infection ◽  
Antiplatelet Agent ◽  
Severe Infections ◽  
Lung Endothelium

ABSTRACTLung injury after influenza infection is characterized by increased permeability of the lung microvasculature, culminating in acute respiratory failure. Platelets interact with activated endothelial cells and have been implicated in the pathogenesis of some forms of acute lung injury. Autopsy studies have revealed pulmonary microthrombi after influenza infection, and epidemiological studies suggest that influenza vaccination is protective against pulmonary thromboembolism; however, the effect of influenza infection on platelet-endothelial interactions is unclear. We demonstrate that endothelial infection with both laboratory and clinical strains of influenza virus increased the adhesion of human platelets to primary human lung microvascular endothelial cells. Platelets adhered to infected cells as well as to neighboring cells, suggesting a paracrine effect. Influenza infection caused the upregulation of von Willebrand factor and ICAM-1, but blocking these receptors did not prevent platelet-endothelial adhesion. Instead, platelet adhesion was inhibited by both RGDS peptide and a blocking antibody to platelet integrin α5β1, implicating endothelial fibronectin. Concordantly, lung histology from infected mice revealed viral dose-dependent colocalization of viral nucleoprotein and the endothelial marker PECAM-1, while platelet adhesion and fibronectin deposition also were observed in the lungs of influenza-infected mice. Inhibition of platelets using acetylsalicylic acid significantly improved survival, a finding confirmed using a second antiplatelet agent. Thus, influenza infection induces platelet-lung endothelial adhesion via fibronectin, contributing to mortality from acute lung injury. The inhibition of platelets may constitute a practical adjunctive strategy to the treatment of severe infections with influenza.IMPORTANCEThere is growing appreciation of the involvement of the lung endothelium in the pathogenesis of severe infections with influenza virus. We have recently shown that the virus can infect human lung endothelial cells, but the functional consequences of this infection are unknown (S. M. Armstrong, C. Wang, J. Tigdi, X. Si, C. Dumpit, S. Charles, A. Gamage, T. J. Moraes, and W. L. Lee, PLoS One 7:e47323, 2012,http://dx.doi.org/10.1371/journal.pone.0047323). Here, we show that this infection causes platelets to adhere to the lung endothelium. Importantly, blocking platelets using two distinct antiplatelet drugs improved survival in a mouse model of severe influenza infection. Thus, platelet inhibition may constitute a novel therapeutic strategy to improve the host response to severe infections with influenza.

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