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Ubiquitous transgenic overexpression of C-C chemokine ligand 2: a model to assess the combined effect of high energy intake and continuous low-grade inflammation.

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2013

Mediators of inflammation 2013;2013:953841. doi: 10.1155/2013/953841. Epub 2013 Dec 15.

Ubiquitous transgenic overexpression of C-C chemokine ligand 2: a model to assess the combined effect of high energy intake and continuous low-grade inflammation.

E Rodríguez-Gallego;M Riera-Borrull;A Hernández-Aguilera;R Mariné-Casadó;A Rull;R Beltrán-Debón;F Luciano-Mateo;JA Menendez;A Vazquez-Martin;JJ Sirvent;V Martín-Paredero;AL Corbí;E Sierra-Filardi;G Aragonès;A García-Heredia;J Camps;C Alonso-Villaverde;J Joven

Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d'Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Carrer Sant Llorenç 21, 43201 Reus, Spain ; Campus of International Excellence Southern Catalonia, Spain. Catalan I

Service type: Transgenic mice

Abstract

Excessive energy management leads to low-grade, chronic inflammation, which is a significant factor predicting noncommunicable diseases. In turn, inflammation, oxidation, and metabolism are associated with the course of these diseases; mitochondrial dysfunction seems to be at the crossroads of mutual relationships. The migration of immune cells during inflammation is governed by the interaction between chemokines and chemokine receptors. Chemokines, especially C-C-chemokine ligand 2 (CCL2), have a variety of additional functions that are involved in the maintenance of normal metabolism. It is our hypothesis that a ubiquitous and continuous secretion of CCL2 may represent an animal model of low-grade chronic inflammation that, in the presence of an energy surplus, could help to ascertain the afore-mentioned relationships and/or to search for specific therapeutic approaches. Here, we present preliminary data on a mouse model created by using targeted gene knock-in technology to integrate an additional copy of the CCl2 gene in the Gt(ROSA)26Sor locus of the mouse genome via homologous recombination in embryonic stem cells. Short-term dietary manipulations were assessed and the findings include metabolic disturbances, premature death, and the manipulation of macrophage plasticity and autophagy. These results raise a number of mechanistic questions for future study.

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