Article
Microglia-secreted galectin-3 acts as a toll-like receptor 4 ligand and contributes to microglial activation
Author/s | Burguillos García, Miguel Ángel
Svensson, Martina Schulte, Tim Boza Serrano, Antonio García Quintanilla, Alberto Kavanagh, Edel T. Santiago Pavón, Martiniano Viceconte, Nikenza Oliva Martín, María José Osman, Ahmed Mohamed Salomonsson, Emma Amar, Lahouari Persson, Annette Blomgren, Klas Achour, Adnane Englund, Elisabet Leffler, Hakon Venero Recio, José Luis Joseph, Bertrand Deierborg, Tomas |
Department | Universidad de Sevilla. Departamento de Bioquímica y Biología Molecular |
Publication Date | 2015 |
Deposit Date | 2016-05-24 |
Published in |
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Abstract | Inflammatory response induced by microglia plays
a critical role in the demise of neuronal populations
in neuroinflammatory diseases. Although the role of
toll-like receptor 4 (TLR4) in microglia’s inflammatory
response ... Inflammatory response induced by microglia plays a critical role in the demise of neuronal populations in neuroinflammatory diseases. Although the role of toll-like receptor 4 (TLR4) in microglia’s inflammatory response is fully acknowledged, little is known about endogenous ligands that trigger TLR4 activation. Here, we report that galectin-3 (Gal3) released by microglia acts as an endogenous paracrine TLR4 ligand. Gal3-TLR4 interaction was further confirmed in a murine neuroinflammatory model (intranigral lipopolysaccharide [LPS] injection) and in human stroke subjects. Depletion of Gal3 exerted neuroprotective and anti-inflammatory effects following global brain ischemia and in the neuroinflammatory LPS model. These results suggest that Gal3-dependent- TLR4 activation could contribute to sustained microglia activation, prolonging the inflammatory response in the brain |
Citation | Burguillos García, M.Á., Svensson, M., Schulte, T., Boza Serrano, A., García Quintanilla, A., Kavanagh, E.T.,...,Deierborg, T. (2015). Microglia-secreted galectin-3 acts as a toll-like receptor 4 ligand and contributes to microglial activation. Cell Reports, 10 (9), 1626-1639. |
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