The effect of aminoguanidine on acute lung injury induced by influenza A/H1N1/PDM09

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
Keyword(s):  
Influenza Virus ◽  
Acute Lung Injury ◽  
Lung Injury ◽  
Influenza A ◽  
Structural Changes ◽  
Saturation Index ◽  
Influenza Infection ◽  
Proinflammatory Response ◽  
Influenza Virus A ◽  
Influenza A H1n1

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.

scholarly journals Influenza A (H1N1): the first hit for transfusion-related acute lung injury?

Critical Care ◽  
2014 ◽  
Vol 18 (Suppl 1) ◽  
pp. P114
Author(s):  
F Piza ◽  
F Carvalho ◽  
H Li ◽  
T Crochemore ◽  
R Rodrigues
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Influenza A ◽  
Influenza A H1n1

scholarly journals IL-17 response mediates acute lung injury induced by the 2009 Pandemic Influenza A (H1N1) Virus

Cell Research ◽  
2011 ◽  
Vol 22 (3) ◽  
pp. 528-538 ◽  
Author(s):  
Chenggang Li ◽  
Penghui Yang ◽  
Yang Sun ◽  
Taisheng Li ◽  
Chen Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Pandemic Influenza ◽  
Influenza A ◽  
H1n1 Virus ◽  
Influenza A H1n1

scholarly journals The Modified JiuWei QiangHuo Decoction Alleviated Severe Lung Injury Induced by H1N1 Influenza Virus by Regulating the NF-κB Pathway in Mice

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Lijuan Chen ◽  
Xin Yan ◽  
Qianlin Yan ◽  
Jiajun Fan ◽  
Hai Huang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Lung Injury ◽  
Influenza A ◽  
H1n1 Virus ◽  
Alternative Therapy ◽  
Severe Pneumonia ◽  
H1n1 Influenza ◽  
Influenza A H1n1 ◽  
Lung Injuries ◽  
Severe Lung

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.

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 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.

scholarly journals Corticosteroid Treatment Ameliorates Acute Lung Injury Induced by 2009 Swine Origin Influenza A (H1N1) Virus in Mice

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e44110 ◽  
Author(s):  
Chenggang Li ◽  
Penghui Yang ◽  
Yanli Zhang ◽  
Yang Sun ◽  
Wei Wang ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Influenza A ◽  
H1n1 Virus ◽  
Corticosteroid Treatment ◽  
Influenza A H1n1

scholarly journals Acute Lung Injury with Alveolar Hemorrhage Due to a Novel Swine-Origin Influenza A (H1N1) Virus

2010 ◽  
Vol 49 (5) ◽  
pp. 427-430 ◽  
Author(s):  
Toshiki Yokoyama ◽  
Kenji Tsushima ◽  
Atsuhito Ushiki ◽  
Nobumitsu Kobayashi ◽  
Kazuhisa Urushihata ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Influenza A ◽  
H1n1 Virus ◽  
Alveolar Hemorrhage ◽  
Influenza A H1n1

scholarly journals Immunogenicity of Modern Vaccine Viruses of Influenza A (H1N1)pdm09 According to Graphical Analysis

2017 ◽  
Vol 16 (5) ◽  
pp. 28-32
Author(s):  
V. S. Vakin ◽  
O. S. Konshina ◽  
E. M. Wojciechowska ◽  
E. V. Kuznetsova ◽  
V. G. Mayorova ◽  
...  
Keyword(s):  
Immune Response ◽  
Influenza Virus ◽  
Influenza A ◽  
Graphical Analysis ◽  
Graphical Form ◽  
Influenza Virus A ◽  
Methods Of Evaluation ◽  
Limited Effectiveness ◽  
Influenza A H1n1 ◽  
Antibody Titers

Antiepidemic measures were limited effectiveness for several years Objectives of this research were formulated as an assessment of the immunogenicity activity of the influenza virus A(H1N1)pdm09 in the composition of modern trivaccines Immunogenicity of the influenza virus A(H1N1)pdm09 in the vaccinated by vaccine was assessed by graphing, reflecting the dynamics of the multiplicity growth of antibodies (MG) and medium ratio of antibodies increasing (MR) in sera for several groups vaccinated. For comparison of vaccinated immunity was determined by traditional methods of evaluation of the immune response. As a result of the research, differences in the immunogenicity activity of the virus were revealed, which are reflected in antibody titers and the multiplicities of their growth from 2 to 4 - 8 times with the applying of similar quality vaccines. These changes couldn’t be observed with accounting study of the immune response. When immunized with a vaccine with an antigen dose of 5 mg HA identified a group of«silent» volunteers (8%) who did not respond to promotion with antigen A(H1N1)pdm09. Increasing dose of the influenza virus A(H1N1)pdm09 to 15 mg/dose in the split vaccine were result of the elimination of the group of«silent» volunteers. Simultaneously was observed a significant increase in the immune response in serum titers (up to 32-fold) and antibody growth rates Accordingly, using of the graphical form of accounting made it possible to better assess the details of the formation of collective immunity to the virus A(H1N1)pdm09 and the nature of its deviations in a number of cases.

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