Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation.
Research output: Contribution to journal › Article
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.
|Research areas and keywords||
Subject classification (UKÄ) – MANDATORY
|Publication status||Published - 2015|
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)
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Related research output
Antonio Boza Serrano, 2017, Lund: Lund University: Faculty of Medicine. 107 p.
Research output: Thesis › Doctoral Thesis (compilation)