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

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 colo...

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Authors: Espinosa-Oliva, Ana María, García-Miranda, Pablo, Alonso-Bellido, Isabel M, Carvajal, Ana E, González-Rodríguez, Melania, Carrillo-Jiménez, Alejandro, Temblador, Arturo J, Felices-Navarro, Manuel, García-Domínguez, Irene, Roca-Ceballos, María Angustias, Vázquez-Carretero, María D, García-Revilla, Juan, Santiago, Marti, Peral, María J, Venero, José Luis, de Pablos, Rocío M
Format: article
Publication Date:2021
Country:España
Institution:Universidad Loyola Andalucía
Repository:Brújula
OAI Identifier:oai:repositorio.uloyola.es:20.500.12412/7049
Online Access:https://hdl.handle.net/20.500.12412/7049
Access Level:Open access
Keyword:Galectin-3
Microglia
Parkinson’s disease
Peripheral inflammation
Neuroinflammation
Description
Summary: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.

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