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


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.


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@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} }