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The expression profiles of immune genes in Mus musculus macrophages during Staphylococcus aureus infection

Staphylococcus aureus is an important pathogen which is often the cause of major morbidity and mortality in both hospital and community settings. For this reason, we investigated the host cell early immune resoponse to S. aureus infection using genome-wide analysis. To do this, we infected Mus muscu...

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Detalles Bibliográficos
Autores principales: Wang, Ziyan, Zhu, Fei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755788/
https://www.ncbi.nlm.nih.gov/pubmed/29304086
http://dx.doi.org/10.1371/journal.pone.0190490
Descripción
Sumario:Staphylococcus aureus is an important pathogen which is often the cause of major morbidity and mortality in both hospital and community settings. For this reason, we investigated the host cell early immune resoponse to S. aureus infection using genome-wide analysis. To do this, we infected Mus musculus RAW264.7 cells with S. aureus alone or in the presence of free peptidoglycan (PG), which appears in the S. aureus cell wall. Post infection, we performed a genome-wide analysis of RAW246.7 cells to identify significant changes in the gene expression profile. Further, we analyzed the infected RAW246.7 cells with transmission electron microscopy looking for the presence of bacterial cells inside the host cell. We also used flow cytometry to determine whether cells had induced apoptosis. The results showed that S. aureus induced apoptosis in the RAW246.7 cells but did not effectively clear away intracellular bacteria cells. However, S. aureus + PG treatment inhibited the apoptosis and activated the host cell inflammation response, possibly involving NF-κB and JAK-STAT pathways, as identified by genome-wide analysis, in RAW246.7 cells. Our study demonstrated for the first time that an independent application of free PG was capable of activating immune responses the host cells.