van Zoelen MA, van der Sluijs KF, Achouiti A, Flor. Receptor for advanced glycation end products is detrimental during influenza A virus pneumonia. Virology. 2009 Jul 8
Pneumonia caused by influenza A virus (IAV) can have devastating effects, resulting in respiratory failure and death. The idea that a new influenza pandemic might occur in the near future has triggered renewed interests in IAV infection. The receptor for advanced glycation end products (RAGE) is expressed on different cell types and plays a key role in diverse inflammatory processes. We here investigated the role of RAGE in the host response to IAV pneumonia using wild-type (wt) and RAGE deficient ((-/-)) mice. Whereas strong RAGE was constitutively expressed in the lungs of uninfected wt mice, in particular on endothelium, IAV pneumonia was associated with enhanced expression on endothelium and de novo expression on bronchial epithelium. Additionally, the high-affinity RAGE ligand high mobility group box 1 was upregulated during IAV pneumonia. RAGE(-/-) mice were relatively protected from IAV induced mortality and showed an improved viral clearance and enhanced cellular T cell response and activation of neutrophils. These data suggest that RAGE is detrimental during IAV pneumonia.
See Also:
Latest articles in those days:
- Nucleic acid detection and genomic sequence analysis of one H5N1 avian influenza virus from wide birds around Qinghai Lake 9 hours ago
- An aggregated dataset of serial morbidity and titer measurements from influenza A virus-infected ferrets 13 hours ago
- Structures of H5N1 influenza polymerase with ANP32B reveal mechanisms of genome replication and host adaptation 3 days ago
- Risk assessment of a highly pathogenic H5N1 influenza virus from mink 3 days ago
- Detection of clade 2.3.4.4b highly pathogenic H5N1 influenza virus in New York City 3 days ago
[Go Top] [Close Window]