Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation.

Miguel Burguillos Garcia, Martina Svensson, Tim Schulte, Antonio Boza Serrano, Albert Garcia-Quintanilla, Edel Kavanagh, Martiniano Santiago, Nikenza Viceconte, Maria Jose Oliva-Martin, Ahmed Mohamed Osman, Emma Salomonsson, Lahouari Amar, Annette Persson, Klas Blomgren, Adnane Achour, Elisabet Englund, Hakon Leffler, Jose Luis Venero, Bertrand Joseph, Tomas Deierborg

Research output: Contribution to journalArticlepeer-review

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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 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.
Original languageEnglish
Pages (from-to)1626-1638
JournalCell Reports
Volume10
Issue number9
DOIs
Publication statusPublished - 2015

Bibliographical note

The information about affiliations in this record was updated in December 2015.
The record was previously connected to the following departments: Neuronal Survival (013212041), Pathology, (Lund) (013030000), Division of Microbiology, Immunology and Glycobiology - MIG (013025200), Neuroinflammation (013210006)

Subject classification (UKÄ)

  • Cell Biology

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