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Mediators of Inflammation
Volume 2013 (2013), Article ID 953841, 19 pages
Research Article

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

1Unitat de Recerca Biomèdica, Hospital Universitari Sant Joan, Institut d’Investigació Sanitària Pere Virgili, Universitat Rovira i Virgili, Carrer Sant Llorenç 21, 43201 Reus, Spain
2Campus of International Excellence Southern Catalonia, Spain
3Catalan Institute of Oncology and Girona Biomedical Research Institute, Avda de Francia s/n, 17007 Girona, Spain
4Department of Pathology, Hospital Universitari Joan XXIII, C/ Dr. Mallafrè Guasch 4, 43005 Tarragona, Spain
5Department of Vascular Surgery, Hospital Universitari Joan XXIII, C/ Dr. Mallafrè Guasch 4, 43005 Tarragona, Spain
6Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Científicas, Ramiro de Maeztu 9, 28040 Madrid, Spain
7Servei de Medicina Interna, Hospital Sant Pau i Santa Tecla, Rambla Vella 14, 43003 Tarragona, Spain

Received 22 July 2013; Revised 30 September 2013; Accepted 15 October 2013

Academic Editor: Donna-Marie McCafferty

Copyright © 2013 Esther Rodríguez-Gallego et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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.