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Title

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

AuthorsMartínez, Isidoro; Oliveros, Juan C.; García, Ernesto ; Garmendia, Juncal ; Menéndez, Margarita ; Nieto, Amelia; Ortín, Juan; Pérez-González, Alicia; Ramos-Sevillano, Elisa ; Rodríguez-Frandsen, Ariel; Solís, Dolores; Yuste, José ; Melero, José A.
KeywordsRespiratory pathogens
Host response
Core of up-regulated genes,
Bacterial infections
Viral infections
Issue Date1-Mar-2017
PublisherFrontiers Media
CitationFrontiers in Microbiology 8: 276 (2017)
AbstractLower 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.
Description13 p.-5 fig.3 tab. Martínez, Isidoro et al.
Publisher version (URL)http://dx.doi.org/10.3389/fmicb.2017.00276
URIhttp://hdl.handle.net/10261/147768
DOI10.3389/fmicb.2017.00276
E-ISSN1664-302X
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