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

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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.

Detaljer

Författare
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Forskningsområden

Ämnesklassifikation (UKÄ) – OBLIGATORISK

  • Cellbiologi
Originalspråkengelska
Sidor (från-till)1626-1638
TidskriftCell Reports
Volym10
Utgivningsnummer9
StatusPublished - 2015
PublikationskategoriForskning
Peer review utfördJa

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Relaterad forskningsoutput

Antonio Boza Serrano, 2017, Lund: Lund University, Faculty of Medicine. 107 s.

Forskningsoutput: AvhandlingDoktorsavhandling (sammanläggning)

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