tetano
Editor, Senior Moderator
J Med Virol. 2013 Nov 8. doi: 10.1002/jmv.23801. [Epub ahead of print]
Transcriptome profiling of brain edemas caused by influenza infection and lipopolysaccharide treatment.
Kyan Y, Ueda Y, Yoshida M, Sasahara K, Shinya K.
Source
Graduate School of Medicine, Kobe University, Hyogo, Japan.
Abstract
Influenza A virus-associated encephalopathy triggered by influenza virus infection often occurs in children aged five and younger in Japan. However, the mechanisms behind Influenza A virus-associated encephalopathy are not yet well understood. This study developed an Influenza A virus-associated encephalopathy-like model using mice infected with Influenza A virus and given lipopolysaccharide treatment. The results showed that the mice used in the model suffered from brain edemas nearly three times more severe, as well as having higher cytokine levels in sera compared to those of the control groups. Using gene expression profiling, cytokine-related genes were found not to be up-regulated in the brain in situ, while protein coding genes, which are known to be involved in blood-brain barrier disruption, were up-regulated. Categorizing the functional groups using gene ontology revealed the terms "ion channels," "calcium oscillation," and "membrane transporter activities." The blood-brain barrier disruption found in this Influenza A virus-associated encephalopathy model can therefore be assumed to be due to a cellular electrolyte imbalance of the neuronal tissue, in addition to a cytokine storm. J. Med. Virol. ? 2013 Wiley Periodicals, Inc.
? 2013 Wiley Periodicals, Inc.
KEYWORDS:
CNS, cytokine storm, electrolyte deficiency, encephalopathy, influenza virus, microarray
PMID:
24306925
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24306925
Transcriptome profiling of brain edemas caused by influenza infection and lipopolysaccharide treatment.
Kyan Y, Ueda Y, Yoshida M, Sasahara K, Shinya K.
Source
Graduate School of Medicine, Kobe University, Hyogo, Japan.
Abstract
Influenza A virus-associated encephalopathy triggered by influenza virus infection often occurs in children aged five and younger in Japan. However, the mechanisms behind Influenza A virus-associated encephalopathy are not yet well understood. This study developed an Influenza A virus-associated encephalopathy-like model using mice infected with Influenza A virus and given lipopolysaccharide treatment. The results showed that the mice used in the model suffered from brain edemas nearly three times more severe, as well as having higher cytokine levels in sera compared to those of the control groups. Using gene expression profiling, cytokine-related genes were found not to be up-regulated in the brain in situ, while protein coding genes, which are known to be involved in blood-brain barrier disruption, were up-regulated. Categorizing the functional groups using gene ontology revealed the terms "ion channels," "calcium oscillation," and "membrane transporter activities." The blood-brain barrier disruption found in this Influenza A virus-associated encephalopathy model can therefore be assumed to be due to a cellular electrolyte imbalance of the neuronal tissue, in addition to a cytokine storm. J. Med. Virol. ? 2013 Wiley Periodicals, Inc.
? 2013 Wiley Periodicals, Inc.
KEYWORDS:
CNS, cytokine storm, electrolyte deficiency, encephalopathy, influenza virus, microarray
PMID:
24306925
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/24306925