How might we best modulate the wound inflammatory response to make skin wounds heal better?
Given our current understanding of the link between inflammation and skin repair, it makes good sense to cautiously begin considering ways in which we might dampen down the inflammatory response in various ways in order to improve the final quality of healing. At a fundamental level, this could be done at several key moments in the inflammatory process (Figure 2): leukocytes could be blocked in the various steps leading to their transmigration from the blood stream through the vessel wall, or their migration from vessel to wound could be blocked, or their activation state could be modulated so they no longer deliver their “fibrotic” message to host wound fibroblasts, or the responding fibroblasts could be blocked in their response to this fibrosis signal. To design therapies that might target any of these steps, it is clearly key to understand the genetic basis of each step, and to a first approximation, we do now have a fair list of the genetic players in diapedesis and the same, at l
