TLR4 activation mediates kidney ischemia/reperfusion injury
The University of Sydney · Royal Prince Alfred Hospital · +1 more institution
Abstract
Ischemia/reperfusion injury (IRI) may activate innate immunity through the engagement of TLRs by endogenous ligands. TLR4 expressed within the kidney is a potential mediator of innate activation and inflammation. Using a mouse model of kidney IRI, we demonstrated a significant increase in TLR4 expression by tubular epithelial cells (TECs) and infiltrating leukocytes within the kidney following ischemia. TLR4 signaling through the MyD88-dependent pathway was required for the full development of kidney IRI, as both TLR4(-/-) and MyD88(-/-) mice were protected against kidney dysfunction, tubular damage, neutrophil and macrophage accumulation, and expression of proinflammatory cytokines and chemokines. In vitro,…
Citation impact
- FWCI
- 30.58
- Percentile
- 100%
- References
- 53
Authors
9- HWHuiling WuCorresponding
The University of Sydney, Royal Prince Alfred Hospital
- GCGang Chen
The University of Sydney, Royal Prince Alfred Hospital
- KWKate Wyburn
The University of Sydney, Royal Prince Alfred Hospital
- JYJianlin Yin
The University of Sydney, Royal Prince Alfred Hospital
- PBPatrick Bertolino
The University of Sydney, Royal Prince Alfred Hospital
Topics & keywords
- TLR4
- Proinflammatory cytokine
- Kidney
- HMGB1
- Renal ischemia
- Chemokine
- Inflammation
- Innate immune system
- Good health and well-being