Galectin-3 Deletion Reduces LPS and Acute Colitis-Induced Pro-Inflammatory Microglial Activation in the Ventral Mesencephalon.

Autor:	Espinosa-Oliva AM; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., García-Miranda P; Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain., Alonso-Bellido IM; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., Carvajal AE; Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain., González-Rodríguez M; Neuroplasticity and Neurodegeneration Laboratory, Ciudad Real Medical School, CRIB, Universidad de Castilla-La Mancha, Ciudad Real, Spain., Carrillo-Jiménez A; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., Temblador AJ; Laboratory of Virology and Chemotherapy, Department of Microbiology, Immunology and Transplantation, Rega Institute for Medical Research, Leuven, Belgium., Felices-Navarro M; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., García-Domínguez I; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., Roca-Ceballos MA; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., Vázquez-Carretero MD; Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain., García-Revilla J; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., Santiago M; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., Peral MJ; Departamento de Fisiología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain., Venero JL; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain., de Pablos RM; Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen Del Rocío/CSIC/Universidad de Sevilla, Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de, Sevilla, Spain.
Jazyk:	angličtina
Zdroj:	Frontiers in pharmacology [Front Pharmacol] 2021 Aug 18; Vol. 12, pp. 706439. Date of Electronic Publication: 2021 Aug 18 (Print Publication: 2021).
DOI:	10.3389/fphar.2021.706439
Abstrakt:	Parkinson's disease is a highly prevalent neurological disorder for which there is currently no cure. Therefore, the knowledge of risk factors as well as the development of new putative molecular targets is mandatory. In this sense, peripheral inflammation, especially the originated in the colon, is emerging as a predisposing factor for suffering this disease. We have largely studied the pleiotropic roles of galectin-3 in driving microglia-associated immune responses. However, studies aimed at elucidating the role of galectin-3 in peripheral inflammation in terms of microglia polarization are lacking. To achieve this, we have evaluated the effect of galectin-3 deletion in two different models of acute peripheral inflammation: intraperitoneal injection of lipopolysaccharide or gut inflammation induced by oral administration of dextran sodium sulfate. We found that under peripheral inflammation the number of microglial cells and the expression levels of pro-inflammatory mediators take place specifically in the dopaminergic system, thus supporting causative links between Parkinson's disease and peripheral inflammation. Absence of galectin-3 highly reduced neuroinflammation in both models, suggesting an important central regulatory role of galectin-3 in driving microglial activation provoked by the peripheral inflammation. Thus, modulation of galectin-3 function emerges as a promising strategy to minimize undesired microglia polarization states. Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. (Copyright © 2021 Espinosa-Oliva, García-Miranda, Alonso-Bellido, Carvajal, González-Rodríguez, Carrillo-Jiménez, Temblador, Felices-Navarro, García-Domínguez, Roca-Ceballos, Vázquez-Carretero, García-Revilla, Santiago, Peral, Venero and de Pablos.)
Databáze:	MEDLINE
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