Regulation of lung injury and repair by Toll-like receptors and hyaluronan

@article{Jiang2005RegulationOL,
  title={Regulation of lung injury and repair by Toll-like receptors and hyaluronan},
  author={Dianhua Jiang and Jiurong Liang and Juan Fan and Shuang Yu and Suping Chen and Yi Luo and Glenn D. Prestwich and Marcella M. Mascarenhas and Hari G. Garg and Deborah A. Quinn and Robert J. Homer and Daniel R. Goldstein and Richard J. Bucala and Patty J. Lee and Ruslan Medzhitov and Paul W. Noble},
  journal={Nature Medicine},
  year={2005},
  volume={11},
  pages={1173-1179}
}
Mechanisms that regulate inflammation and repair after acute lung injury are incompletely understood. The extracellular matrix glycosaminoglycan hyaluronan is produced after tissue injury and impaired clearance results in unremitting inflammation. Here we report that hyaluronan degradation products require MyD88 and both Toll-like receptor (TLR)4 and TLR2 in vitro and in vivo to initiate inflammatory responses in acute lung injury. Hyaluronan fragments isolated from serum of individuals with… Expand
Matrix regulation of lung injury, inflammation, and repair: the role of innate immunity.
  • P. Noble, D. Jiang
  • Biology, Medicine
  • Proceedings of the American Thoracic Society
  • 2006
TLDR
It is found that Toll-like receptors 2 and 4 (TLR2 and TLR4) are responsible for macrophage inflammatory gene expression in response to hyaluronan fragments, and they have a protective role against lung injury on alveolar epithelial cells. Expand
The role of Toll-like receptors in non-infectious lung injury
TLDR
It is identified that host matrix component HA and TLR interactions provide signals that initiate inflammatory responses, maintain epithelial cell integrity, and promote recovery from acute lung injury. Expand
Hyaluronan in tissue injury and repair.
TLDR
The interactions between the endogenous matrix component hyaluronan and its signaling receptors initiate inflammatory responses, maintain structural cell integrity, and promote recovery from tissue injury. Expand
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TLDR
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Hyaluronan ameliorates LPS-induced acute lung injury in mice via Toll-like receptor (TLR) 4-dependent signaling pathways.
TLDR
The findings suggest that HA pretreatment attenuated LPS-induced ALI and the anti-inflammatory function of HA was partial dependent on TLR4, which shed new light on potential elements that regulate the lung injury response. Expand
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TLDR
Differential TLR signaling and MAPK activation in response to LIRI seem to be cell specific, and short interference RNA provides an outstanding tool for examination of the underlying mechanism. Expand
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TLDR
It is found that TLR2 is markedly upregulated on tubular and tubulointerstitial cells in patients with chronic renal injury and that the absence ofTLR2 does not affect the development of chronic renal Injury and fibrosis. Expand
Hyaluronan and TLR4 promote surfactant-protein-C-positive alveolar progenitor cell renewal and prevent severe pulmonary fibrosis in mice
TLDR
Evidence is provided that expression of the innate immune receptor Toll-like receptor 4 (TLR4) and the extracellular matrix glycosaminoglycan hyaluronan (HA) on AEC2s are important for A EC2 renewal, repair of lung injury and limiting the extent of fibrosis. Expand
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TLDR
The findings support that ozone-induced airway hyperresponsiveness is dependent on the HA-TLR4-MyD88-TIRAP signaling pathway. Expand
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TLDR
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