期刊
NATURE IMMUNOLOGY
卷 6, 期 9, 页码 902-910出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1233
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资金
- NHLBI NIH HHS [HL23594, HL57345, P01 HL057345] Funding Source: Medline
- NIAID NIH HHS [AI50498, R01 AI035796, AI35796] Funding Source: Medline
- NIGMS NIH HHS [GM33063] Funding Source: Medline
Here we have studied the involvement of endothelial heparan sulfate in inflammation by inactivating the enzyme N- acetyl glucosamine N- deacetylase - N- sulfotransferase- 1 in endothelial cells and leukocytes, which is required for the addition of sulfate to the heparin sulfate chains. Mutant mice developed normally but showed impaired neutrophil infiltration in various inflammation models. These effects were due to changes in heparan sulfate specifically in endothelial cells. Decreased neutrophil infiltration was partially due to altered rolling velocity correlated with weaker binding of L- selectin to endothelial cells. Chemokine transcytosis across endothelial cells and presentation on the cell surface were also reduced, resulting in decreased neutrophil firm adhesion and migration. Thus, endothelial heparan sulfate has three functions in inflammation: by acting as a ligand for L- selectin during neutrophil rolling; in chemokine transcytosis; and by binding and presenting chemokines at the lumenal surface of the endothelium.
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