%0 Journal Article %A Martínez, Isidoro %A Oliveros, Juan %A Cuesta, Isabel %A Barrera, Jorge %A Ausina, Vicente %A Casals Carro, María Cristina %A Lorenzo, Alba de %A García, Ernesto %A García-Fojeda García-Valdecasas, María Belén %A Garmendia, Junkal %A González-Nicolau, Mar %A Lacoma, Alicia %A Menéndez, Margarita %A Moranta, David %A Nieto, Amelia %A Ortín, Juan %A Pérez-González, Alicia %A Prat, Cristina %A Ramos-Sevillano, Elisa %A Regueiro, Verónica %A Rodriguez-Frandsen, Ariel %A Solís, Dolores %A Yuste, José %A Bengoechea, José %A Melero, José %T Apoptosis, Toll-like, RIG-I-like and NOD-like Receptors Are Pathways Jointly Induced by Diverse Respiratory Bacterial and Viral Pathogens %D 2017 %@ 1664-302X %U https://hdl.handle.net/20.500.14352/94519 %X 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. %~