tetano
Editor, Senior Moderator
Crit Care. 2012 Aug 16;16(4):R157. [Epub ahead of print]
A distinct influenza infection signature in the blood transcriptome of patients who presented with severe community acquired pneumonia.
Parnell GP, McLean AS, Booth DR, Armstrong NJ, Nalos M, Huang SJ, Manak J, Tang W, Tam OY, Chan S, Tang BM.
Abstract
ABSTRACT:
INTRODUCTION:
Diagnosis of severe influenza pneumonia remains challenging because there is a lack of correlation between the presence of influenza virus and clinical status. We conducted gene expression profiling in the whole blood of critically ill patients to identify a gene signature that would allow clinicians to distinguish influenza infection from other causes of severe respiratory failure, such as bacterial pneumonia, and non-infective systemic inflammatory response syndrome.
METHODS:
Whole blood samples were collected from critically ill individuals and assayed on Illumina HT-12 gene expression beadarrays. Differentially expressed genes were determined by linear mixed model analysis and over-represented biological pathways determined using GeneGo MetaCore.
RESULTS:
The gene expression profile of H1N1 influenza A pneumonia was distinctly different from bacterial pneumonia and systemic inflammatory response syndrome. The influenza gene expression profile is characterized by up-regulation of genes from cell cycle regulation, apoptosis and DNA-damage response pathways. In contrast, no distinctive gene-expression signature was found in patients with bacterial pneumonia or systemic inflammatory response syndrome. The gene expression profile of influenza infection persisted through 5 days of follow-up. Furthermore, in patients with primary H1N1 influenza A infection who subsequently developed bacterial co-infection, the influenza gene-expression signature remained unaltered, despite the presence of a super-imposed bacterial infection.
CONCLUSIONS:
The whole blood expression profiling data indicates that the host response to influenza pneumonia is distinctly different from that caused by bacterial pathogens. This information may speed up identification of the cause of infection in patients presenting with severe respiratory failure, allowing appropriate patient care to be undertaken more rapidly.
PMID:
22898401
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22898401
A distinct influenza infection signature in the blood transcriptome of patients who presented with severe community acquired pneumonia.
Parnell GP, McLean AS, Booth DR, Armstrong NJ, Nalos M, Huang SJ, Manak J, Tang W, Tam OY, Chan S, Tang BM.
Abstract
ABSTRACT:
INTRODUCTION:
Diagnosis of severe influenza pneumonia remains challenging because there is a lack of correlation between the presence of influenza virus and clinical status. We conducted gene expression profiling in the whole blood of critically ill patients to identify a gene signature that would allow clinicians to distinguish influenza infection from other causes of severe respiratory failure, such as bacterial pneumonia, and non-infective systemic inflammatory response syndrome.
METHODS:
Whole blood samples were collected from critically ill individuals and assayed on Illumina HT-12 gene expression beadarrays. Differentially expressed genes were determined by linear mixed model analysis and over-represented biological pathways determined using GeneGo MetaCore.
RESULTS:
The gene expression profile of H1N1 influenza A pneumonia was distinctly different from bacterial pneumonia and systemic inflammatory response syndrome. The influenza gene expression profile is characterized by up-regulation of genes from cell cycle regulation, apoptosis and DNA-damage response pathways. In contrast, no distinctive gene-expression signature was found in patients with bacterial pneumonia or systemic inflammatory response syndrome. The gene expression profile of influenza infection persisted through 5 days of follow-up. Furthermore, in patients with primary H1N1 influenza A infection who subsequently developed bacterial co-infection, the influenza gene-expression signature remained unaltered, despite the presence of a super-imposed bacterial infection.
CONCLUSIONS:
The whole blood expression profiling data indicates that the host response to influenza pneumonia is distinctly different from that caused by bacterial pathogens. This information may speed up identification of the cause of infection in patients presenting with severe respiratory failure, allowing appropriate patient care to be undertaken more rapidly.
PMID:
22898401
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22898401