Apoptosis, toll-like, RIG-I-like and NOD-like receptors are pathways jointly induced by diverse respiratory bacterial and viral pathogens

3Citations
Citations of this article
40Readers
Mendeley users who have this article in their library.

Abstract

Lower respiratory tract infections are among the top five leading causes of human death. Fighting these infections is therefore a world health priority. Searching for induced alterations in host gene expression shared by several relevant respiratory pathogens represents an alternative to identify new targets for wide-range host-oriented therapeutics. With this aim, alveolar macrophages were independently infected with three unrelated bacterial (Streptococcus pneumoniae, Klebsiella pneumoniae, and Staphylococcus aureus) and two dissimilar viral (respiratory syncytial virus and influenza A virus) respiratory pathogens, all of them highly relevant for human health. Cells were also activated with bacterial lipopolysaccharide (LPS) as a prototypical pathogen-associated molecular pattern. Patterns of differentially expressed cellular genes shared by the indicated pathogens were searched by microarray analysis. Most of the commonly up-regulated host genes were related to the innate immune response and/or apoptosis, with Toll-like, RIG-I-like and NOD-like receptors among the top 10 signaling pathways with over-expressed genes. These results identify new potential broad-spectrum targets to fight the important human infections caused by the bacteria and viruses studied here.

Cite

CITATION STYLE

APA

Martínez, I., Oliveros, J. C., Cuesta, I., de la Barrera, J., Ausina, V., Casals, C., … Melero, J. A. (2017). Apoptosis, toll-like, RIG-I-like and NOD-like receptors are pathways jointly induced by diverse respiratory bacterial and viral pathogens. Frontiers in Microbiology, 8(MAR). https://doi.org/10.3389/fmicb.2017.00276

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free