in healthy people ordinarily heal without problems and
do not require special medication unless they are infected.
On the other hand, large groups of patients suffer from
chronic wounds which heal very slowly or not at all. Among
them are diabetics, or patients with venous or pressure
ulcers. It was found recently that MALP-2 stimulates
wound closure in an animal model using obese, diabetic
mice. MALP-2 accomplishes accelerated wound closure
in these animals by enhancing the inflammatory phase of
This is brought about by first stimulating the release
of chemokines from skin fibroblasts and keratinocytes.
Chemokines are proteins which attract macrophages and
other leukocytes to the wound. When the macrophages arrive
in the wound, they are stimulated by MALP-2 to
release a cocktail of growth factors and other mediators
required for optimal wound healing. A phase 1 clinical
trial has been carried out after approval by the ethics
committee and showed that MALP-2 was well tolerated
in doses which are expected to be effective. Moreover,
MALP-2 was active in patients with diabetes.
cryosection through the skin of an obese mouse which has been treated
with MALP-2 13 days earlier. The wound edge is shown at the
left, the epidermis at the top. Note the thick fat layer showing
as round "empty" areas to the right.
The red stain is caused by antibodies against CD31, an antigen specific
for endothelial cells. See the many newly formed blood vessels at
the wound edge. Untreated wounds show a much less pronounced neovascularization.