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Heparan sulfate and inflammation

Nature Immunology volume 6, pages 861–862 (2005)Cite this article

Entry of leukocytes into tissues is a key feature of inflammation. New data suggest the polysaccharide heparan sulfate is required for several stages of this entry process.

Heparan sulfate is a ubiquitously expressed polysaccharide that appears on cell surfaces and in extracellular matrices as a proteoglycan. It shows great structural diversity and has been implicated in numerous biological processes1,2. In the case of inflammation, heparan sulfate is a potential ligand for P- and L-selectin, two key molecules involved in the adhesion of leukocytes to inflamed endothelium3. Similarly, heparan sulfate can bind proinflammatory chemokines, transport them across the endothelium and present them to leukocytes3,4. Until now, however, the precise role of heparan sulfate during in vivo inflammatory responses has been unclear. In this issue of Nature Immunology, Wang et al.5 show that endothelial cells expressing partially sulfated heparan sulfate are unable to recruit leukocytes into inflammatory sites. This effect is due to heparan sulfate being an essential adhesion ligand for L-selectin and being required for the transport of chemokines across the endothelial barrier for presentation to leukocytes. In contrast, leukocytes expressing partially sulfated heparan sulfate were unimpaired in their response to inflammatory stimuli. Overall these findings unequivocally demonstrate that endothelial cell expression of heparan sulfate is essential for multiple stages of an inflammatory response.

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Figure 1: Role of heparan sulfate in leukocyte entry into sites of inflammation.

Katie Ris

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Acknowledgements

The author thanks the National Health and Medical Research Council of Australia for support.

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  1. John Curtin School of Medical Research, Australian National University, Canberra, 2601, Australian Capital Territory, Australia

    Christopher R Parish

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  1. Christopher R Parish
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Parish, C. Heparan sulfate and inflammation. Nat Immunol 6, 861–862 (2005). https://doi.org/10.1038/ni0905-861

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  • DOI: https://doi.org/10.1038/ni0905-861

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