Delayed wound healing and disorganized neovascularization in transgenic mice expressing the IP-10 chemokine.

Abstract

IP-10 is a member of the alpha or cysteine-X amino acid-cysteine (CXC) chemokine family of chemotactic cytokines. High levels of IP-10 expression have been detected in a number of chronic human inflammatory conditions, including psoriasis, a common inflammatory disease of the skin. IP-10 has been shown to chemoattract activated T cells, inhibit the proliferation of endothelial cells, and inhibit the growth of tumors in vivo. To determine the capacity of IP-10 to modulate the inflammatory response in vivo, we have created transgenic mice that constitutively express IP-10 from keratinocytes. These mice developed normally and, in general, did not spontaneously recruit leukocytes into the skin or other organs that expressed the transgene. In addition, the transgenic mice had a normal cutaneous contact hypersensitivity cellular immune response. However, IP-10 transgenic mice had an abnormal wound healing response characterized by a more intense inflammatory phase and a prolonged and disorganized granulation phase with impaired blood vessel formation. These results have demonstrated that IP-10 can inhibit the neovascularization associated with a physiological response in vivo and have revealed a novel biologic activity of IP-10 as an inhibitor of wound healing.

Statistics

0204060'00'02'04'06'08'10'12'14'16
Citations per Year

225 Citations

Semantic Scholar estimates that this publication has 225 citations based on the available data.

See our FAQ for additional information.

Cite this paper

@article{Luster1998DelayedWH, title={Delayed wound healing and disorganized neovascularization in transgenic mice expressing the IP-10 chemokine.}, author={Andrew D Luster and Robert Cardiff and James A Maclean and Karen Crowe and Richard D. Granstein}, journal={Proceedings of the Association of American Physicians}, year={1998}, volume={110 3}, pages={183-96} }