Cutaneous wound healing is associated with an initial inflammatory response followed by reformation of the outermost layer of the skin. During this initial response, recruitment of inflammatory cells to the wound site induces increased local expression of MIF, which in turn attracts more inflammatory cells to the site. Ashcroft and colleagues demonstrated that subsequent to small cutaneous incisions, estrogen-deficient mice experienced a local unchecked increase in MIF expression that resulted in excessive inflammation and delayed wound healing.
Furthermore, MIF-deficient mice in the absence of estrogen showed no significant differences in the rate of healing when compared with control mice.
The data implicate MIF as a crucial intermediary in uncontrolled inflammation and impaired healing, suggesting that impaired wound healing could be accelerated with therapeutics that inhibit MIF.
AUTHOR CONTACT:
Gillian S. Ashcroft
University of Manchester, School of Biological Sciences, Manchester, Great Britain
Phone: 44-161-275-5673
Fax: 44-161-275-3915
E-mail: gillian.s.ashcroft@man.ac.uk
View the PDF of this article at: https://www.the-jci.org/press/16288.pdf
Journal of Clinical Investigation