Abstract
Our objective is to study the role of cutaneous Langerhans cells on a mouse model of nicotinic acid-induced vasodilatation. Nicotinic acid-induced vasodilatation was studied in the mouse ear by laser Doppler flowmetry prior to and at intervals after Langerhans cells depletion by treatment with hydrocortisone. Nicotinic acid evoked a dose-dependent increase in perfusion in the mouse ear. Treatment with 1 % hydrocortisone resulted in substantial depletion of Langerhans cells, accompanied by failure to show vasodilatation in response to nicotinic acid. Partial recovery of Langerhans cells on day 53 post-treatment was associated with a partial vasodilatation response. To exclude non-specific effects of hydrocortisone on arachidonic acid metabolism, the ability of the mice to mount an edema response to phorbol 12-myristate 13-acetate was evaluated. On day 9 post hydrocortisone, phorbol 12-myristate 13-acetate failed to evoke an edema response. However, on day 22 post hydrocortisone, the edema response in the hydrocortisone-treated animals was indistinguishable from that of control animals. These results suggest that Langerhans cells are responsible for nicotinic acid-induced vasodilatation.
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