Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: Influenza A viruses cause epidemics and pandemics with damaging health and economic impacts. Alike any obligate intracellular pathogen, IAVs hijack host cell machinery and energetic resources to multiply within, and eventually exit, the host. Increased fatty acid and cholesterol synthesis, as well as increased glucose metabolism have been identified as the major metabolic changes induced by infection. Besides these effects on metabolism, IAV infection also triggers a variety of innate defense mechanisms within the host cell. Although mainly defined as a virus of the respiratory tract, with airway epithelial cells being its prime cellular habitat, complications outside the site of infection have also been reported. However, whether influenza on its own may impact on endocrine tissues and, thereby, lead to metabolic complications, has never been investigated. Here, we compared the response of preadipocytes and adipocytes to IAV infection, in terms of transcriptomic profiles and bioenergetics. The results showed that IAV triggers a browning adipogenesis process, leading to metabolic reprogramming of the adipose tissue resulting in long-lasting alterations of body metabolism. We conclude that the adipose tissue might be an undervalued organ in influenza pathophysiology.

ORGANISM(S): Mus musculus

SUBMITTER: Ronan Le Goffic

PROVIDER: E-MTAB-6646 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Miao2010 - Innate and adaptive immune responses to primary Influenza A Virus infection This model is described in the article: Quantifying the early immune response and adaptive immune response kinetics in mice infected with influenza A virus. Miao H, Hollenbaugh JA, Zand MS, Holden-Wiltse J, Mosmann TR, Perelson AS, Wu H, Topham DJ. J. Virol. 2010 Jul; 84(13): 6687-6698 Abstract: Seasonal and pandemic influenza A virus (IAV) continues to be a public health threat. However, we lack a detailed and quantitative understanding of the immune response kinetics to IAV infection and which biological parameters most strongly influence infection outcomes. To address these issues, we use modeling approaches combined with experimental data to quantitatively investigate the innate and adaptive immune responses to primary IAV infection. Mathematical models were developed to describe the dynamic interactions between target (epithelial) cells, influenza virus, cytotoxic T lymphocytes (CTLs), and virus-specific IgG and IgM. IAV and immune kinetic parameters were estimated by fitting models to a large data set obtained from primary H3N2 IAV infection of 340 mice. Prior to a detectable virus-specific immune response (before day 5), the estimated half-life of infected epithelial cells is approximately 1.2 days, and the half-life of free infectious IAV is approximately 4 h. During the adaptive immune response (after day 5), the average half-life of infected epithelial cells is approximately 0.5 days, and the average half-life of free infectious virus is approximately 1.8 min. During the adaptive phase, model fitting confirms that CD8(+) CTLs are crucial for limiting infected cells, while virus-specific IgM regulates free IAV levels. This may imply that CD4 T cells and class-switched IgG antibodies are more relevant for generating IAV-specific memory and preventing future infection via a more rapid secondary immune response. Also, simulation studies were performed to understand the relative contributions of biological parameters to IAV clearance. This study provides a basis to better understand and predict influenza virus immunity. This model is hosted on BioModels Database and identified by: BIOMD0000000546. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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

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