Chemokine ligand–receptor interactions critically regulate cutaneous wound healing

Table 2 Chemokines enhance wound repair in vitro

ng/ml	Endothelial cells				Fibroblasts				Keratinocytes
ng/ml	10	100	500	1000	10	100	500	1000	10	100	500	1000
CCL1/I-309	40%	40%	60%	n.d.	n.d.	n.d.	n.d.	n.d.	n.d.	n.d.	n.d.	n.d.
CCL3/MIP-1α	×	×	×	×	–	–	–	–	×	×	×	×
CCL11/eotaxin	–	50%	100%	80%	30%	30%	50%	–	40%	40%	70%	60%
CCL17/TARC	–	–	–	n.d.	50%	60%	50%	–	–	70%	40%	30%
CCL20/MIP-3α	–	–	–	n.d.	×	×	×	×	100%	80%	60%	30%
CCL27/CTACK	–	40%	100%	80%	100%	70%	50%	80%	–	–	–	n.d.
CXCL8/IL-8	40%	–	–	n.d.	×	×	×	×	50%	80%	70%	80%
CXCL10/IP-10	–	–	–	n.d.	×	×	×	×	–	20%	80%	100%

Wound repair of single path wounds in confluent cultures of human primary dermal microvascular endothelial cells, dermal fibroblasts and epidermal keratinocytes in the presence of indicated chemokines was monitored 12–18 h after injury. Percentage of wound closure was normalized to medium alone. Experiments were performed in triplicates and representative results of three different donors are shown. (−, closure of wound under 10%; n.d., not determined; ×, no receptor expressed for this ligand)

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