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Burguillos MA, Svensson M, Schulte T, et al. Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation. Cell Rep. 2015;10(9):1626-1638doi: 10.1016/j.celrep.2015.02.012.
Burguillos, M. A., Svensson, M., Schulte, T., Boza-Serrano, A., Garcia-Quintanilla, A., Kavanagh, E., Santiago, M., Viceconte, N., Oliva-Martin, M. J., Osman, A. M., Salomonsson, E., Amar, L., Persson, A., Blomgren, K., Achour, A., Englund, E., Leffler, H., Venero, J. L., Joseph, B., & Deierborg, T. (2015). Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation. Cell reports, 10(9), 1626-1638. https://doi.org/10.1016/j.celrep.2015.02.012
Burguillos, Miguel Angel, et al. "Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation." Cell reports vol. 10,9 (2015): 1626-1638. doi: https://doi.org/10.1016/j.celrep.2015.02.012
Burguillos MA, Svensson M, Schulte T, Boza-Serrano A, Garcia-Quintanilla A, Kavanagh E, Santiago M, Viceconte N, Oliva-Martin MJ, Osman AM, Salomonsson E, Amar L, Persson A, Blomgren K, Achour A, Englund E, Leffler H, Venero JL, Joseph B, Deierborg T. Microglia-Secreted Galectin-3 Acts as a Toll-like Receptor 4 Ligand and Contributes to Microglial Activation. Cell Rep. 2015 Mar 10;10(9):1626-1638. doi: 10.1016/j.celrep.2015.02.012. Epub 2015 Mar 05. PMID: 25753426.
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Cell Rep. 2015 Mar 10;10(9):1626-1638. doi: 10.1016/j.celrep.2015.02.012. Epub 2015 Mar 05.

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

Cell reports

Miguel Angel Burguillos, 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

Affiliations

  1. Department of Oncology-Pathology, Cancer Centrum Karolinska, R8:03, Karolinska Institutet, Stockholm 171 76, Sweden; Experimental Neuroinflammation Laboratory, Department of Experimental Medical Science, Lund University, BMC B11, Lund 221 84, Sweden. Electronic address: [email protected].
  2. Experimental Neuroinflammation Laboratory, Department of Experimental Medical Science, Lund University, BMC B11, Lund 221 84, Sweden.
  3. Science for Life Laboratory, Department of Medicine Solna, Karolinska Institutet, Stockholm 17165, Sweden.
  4. Departamento de Bioquímica y Biología Molecular, Facultad de Farmacia, Universidad de Sevilla and Instituto de Biomedicina de Sevilla (IBiS), Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla, Sevilla 41012, Spain.
  5. Department of Oncology-Pathology, Cancer Centrum Karolinska, R8:03, Karolinska Institutet, Stockholm 171 76, Sweden.
  6. Department of Women's and Children's Health, Karolinska Institutet, Karolinska University Hospital, Q2:07, Stockholm 171 76, Sweden.
  7. Section MIG, Department of Laboratory Medicine, Solvegatan 23, Lund University, Lund 223 62, Sweden.
  8. Neuronal Survival Unit, Department of Experimental Medical Science, Wallenberg Neuroscience Center, Lund University, Lund 221 84, Sweden.
  9. Department of Pathology, Division of Neuropathology, Lund University Hospital, Lund 221 85, Sweden.

PMID: 25753426 DOI: 10.1016/j.celrep.2015.02.012

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.

Copyright © 2015 The Authors. Published by Elsevier Inc. All rights reserved.

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