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

نویسندگان

  • 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
چکیده

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.

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عنوان ژورنال:
  • Cell reports

دوره   شماره 

صفحات  -

تاریخ انتشار 2015