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Influenza infection rewires energy metabolism and induces browning features in adipose cells and tissues

Like all obligate intracellular pathogens, influenza A virus (IAV) reprograms host cell’s glucose and lipid metabolism to promote its own replication. However, the impact of influenza infection on white adipose tissue (WAT), a key tissue in the control of systemic energy homeostasis, has not been ye...

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Detalles Bibliográficos
Autores principales: Ayari, Asma, Rosa-Calatrava, Manuel, Lancel, Steve, Barthelemy, Johanna, Pizzorno, Andrés, Mayeuf-Louchart, Alicia, Baron, Morgane, Hot, David, Deruyter, Lucie, Soulard, Daphnée, Julien, Thomas, Faveeuw, Christelle, Molendi-Coste, Olivier, Dombrowicz, David, Sedano, Laura, Sencio, Valentin, Le Goffic, Ronan, Trottein, François, Wolowczuk, Isabelle
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7224208/
https://www.ncbi.nlm.nih.gov/pubmed/32409640
http://dx.doi.org/10.1038/s42003-020-0965-6
Descripción
Sumario:Like all obligate intracellular pathogens, influenza A virus (IAV) reprograms host cell’s glucose and lipid metabolism to promote its own replication. However, the impact of influenza infection on white adipose tissue (WAT), a key tissue in the control of systemic energy homeostasis, has not been yet characterized. Here, we show that influenza infection induces alterations in whole-body glucose metabolism that persist long after the virus has been cleared. We report depot-specific changes in the WAT of IAV-infected mice, notably characterized by the appearance of thermogenic brown-like adipocytes within the subcutaneous fat depot. Importantly, viral RNA- and viral antigen-harboring cells are detected in the WAT of infected mice. Using in vitro approaches, we find that IAV infection enhances the expression of brown-adipogenesis-related genes in preadipocytes. Overall, our findings shed light on the role that the white adipose tissue, which lies at the crossroads of nutrition, metabolism and immunity, may play in influenza infection.