Present address: Institute of Clinical Pharmacology Parexel International GmbH, Spandauer Damm 130, 14050 Berlin, Germany.
Comparative transcriptional profiling of the lung reveals shared and distinct features of Streptococcus pneumoniae and influenza A virus infection
Article first published online: 8 DEC 2006
Volume 120, Issue 3, pages 380–391, March 2007
How to Cite
Rosseau, S., Hocke, A., Mollenkopf, H., Schmeck, B., Suttorp, N., Kaufmann, S. H. E. and Zerrahn, J. (2007), Comparative transcriptional profiling of the lung reveals shared and distinct features of Streptococcus pneumoniae and influenza A virus infection. Immunology, 120: 380–391. doi: 10.1111/j.1365-2567.2006.02514.x
This article has an online supplement.
- Issue published online: 20 DEC 2006
- Article first published online: 8 DEC 2006
- Received 12 July 2006; revised 6 October 2006; accepted 6 October 2006.
Pneumonia is the most common cause of death from infectious disease in the western hemisphere. Pathophysiological and protective processes are initiated by pattern recognition of microbial structures. To provide the molecular framework for a better understanding of processes relevant to host defence in pneumonia, we performed pulmonary transcriptome analysis in mice infected with the major bacterial and viral agents of community-acquired pneumonia, Streptococcus pneumoniae and influenza A virus. We detected differential expression of 1300 genes after infection with either pathogen. Of these, approximately 36% or 30% were specific for pneumococcal or influenza infection, respectively, yielding pathogen-specific as well as shared inflammatory transcriptional signatures. These results not only reveal a differential response on the cytokine and chemokine levels but also emphasize the important role of genes implicated in regulation and fine tuning of inflammation. As one, albeit unexpected, key feature of pneumococcal pneumonia we discovered down-regulation of B-cell responses, probably reflecting a pneumococcal virulence strategy. The pathophysiological consequences of influenza A virus infection were reflected by the emerging protective T-cell response and differential induction of genes involved in tissue regeneration and proliferation. These data provide new insights into pathogenesis of the most common forms of pneumonia, highlighting the value of transcriptional profiling for the elucidation of underlying mechanisms.