ENDOGENOUS INFLAMMATORY RESPONSE TO DERMAL WOUND-HEALING IN THE FETALAND ADULT-MOUSE

The recruitment of inflammatory cells to a wound may play an important role in the resulting cellular processes and ultimately the quality o f the healing response in the fetus (scar-free healing) or the adult ( scar-forming healing). Using a range of antibodies to monocytes and ma crophages and also to different activation markers of activated macrop hages, we have compared the inflammatory profile of scar-free healing E16 mouse fetal wounds to those of scarring adult wounds. In the fetal wound, small numbers of monocyte derived cells (MOMA-2 and F4/80 posi tive) are recruited to the wound by 3 hr post-wounding. No Mac-1 posit ive cells indicative of activated macrophages were observed until 18 h r post-wounding. Eventually all types of macrophages studied were recr uited to both adult and fetal wound sites but the numbers and persiste nce of these cells are lower in the fetus than in the adult. B cells w ere detected in healing adult wounds but not in the fetal wounds. This absence of H-21-A positive (B) cells in murine fetal wounds could be associated with the low levels of activated Mac-1 positive macrophages at the murine fetal wound site. Activated macrophages in addition to releasing growth factors may also release signals to recruit B cells. Thus, the E16 mouse fetus can mount an inflammatory response to woundi ng. This response differs from that of the adult in the numbers of inf lammatory cells recruited to the wound and the subpopulations of activ ated cells found at the wound site. This study indicates that there ar e complex differences between the in flammatory responses elicited in adult and fetal murine dermal wounds. These differences may determine the profile of growth factors and cytokines released at fetal and adul t wound sites. Manipulation of either the numbers or the activation st ates of inflammatory cells at the adult wound site may be an approach to the control of scarring during adult wound healing. Dev. Dyn. 1998; 212:385-393. (C) 1998 Wiley-Liss, Inc.