Journal of the American Academy of Dermatology
726 Brief communications vasodilation, enhancement of epidermal and endothelial cell proliferation, and release ofinflammatory mediators from macrophages and T lymphocytes).2 The potent vasoclilatory properties of SP originate from the effects of secondary mediators, such as histamine and platelet-activating factor, whose release is triggered by SP,s In addition, SP acts as a mediator of antidromic vasodilation.6 In this preliminary study, we investigated SP immunoreactivity in patients with rosacea to evaluate a possible role of this neuropeptide in its pathogenesis. Patients and methods. Five patients (three women, two men; mean age 43 years) and three volunteers with rosacea (three women; mean age 40 years) were included in the study. The lesions were located in the central portion ofthe face and consisted of erythema, telangiectases, papules, and pustules. After local anesthesia, a 4 mm punch biopsy specimen was taken of an edematous, erythematous papule in each patient and from normal facial skin of volunteers with rosacea in similar locations. Skin samples were immersed in 4% paraformaldehyde solution that contained O.3%pitricacid and fixed at 4° Cfor4 hours. The specimens were then rinsed overnight in phosphate-buffered saline. Frozen sections, 14 limin thickness, were cut and incubated with primary antibody (1:400 dilution) for 48 hours at 4° C. Later, the sections were reincubated with 1:80 dilution of tetramethyl rhodamine isothiocyanate-conjugated goat antirabbit antibody (Boehringer Mannheim) for 30 minutes at 37° C. Between different steps, the sections were rinsed in phosphate-buffered saline for 15 minutes. The antiserum was diluted in phosphate-buffered saline containing 0.3%TritonX-IOO. The antiserum against SP was obtained from Peninsula Laboratories, Belmont, New York.
Results. A blinded reading of the specimens showed that SP-immunoreactive nerves were increased considerably around the blood vessels in the papillary dermis in lesional skin as compared with normal skin. Discussion. Rosacea is a chronic inflammatory skin disease of unknown origin. Vascular dilation, which is a characteristic feature of the disease, has not been adequately explained. The affected skin shows a normal response to mediators such as acetylcholine and there is no evidence ofvascular instability after cooling ofthe skin?' 8 The association between rosacea and migraine seems to be evidence for a primary vascular disease. In addition, vessel malfunction that causes leakage and inflammation has been postulated in the origin of the disease. 8 SP l which has potent vasodilatory activity, could be involved in the vascular dilation of rosacea. We speculate that in a genetically predisposed person, SP released from cutaneous sensory neurons may give rise to vascular dilation and a perivascular inflammatory infiltrate that may be operative in the induction and/or maintenance of rosacea.
REFERENCES I. Naukkarinen A, NickolotfBJ, Farber EM. Quantification of cutaneous sensory nerves and their substance P content in psoriasis. J Invest DermatoI1989;92:126-9.
2. Farber EM, Lanigan SW, Boer J. The role of cutaneous sensory nerves in the maintenance of psoriasis. Int 1 Dermato11990;29:418-20. 3. Kiil'k9iioglu N,
726 Brief communications vasodilation, enhancement of epidermal and endothelial cell proliferation, and release ofinflammatory mediators from macrophages and T lymphocytes).2 The potent vasoclilatory properties of SP originate from the effects of secondary mediators, such as histamine and platelet-activating factor, whose release is triggered by SP,s In addition, SP acts as a mediator of antidromic vasodilation.6 In this preliminary study, we investigated SP immunoreactivity in patients with rosacea to evaluate a possible role of this neuropeptide in its pathogenesis. Patients and methods. Five patients (three women, two men; mean age 43 years) and three volunteers with rosacea (three women; mean age 40 years) were included in the study. The lesions were located in the central portion ofthe face and consisted of erythema, telangiectases, papules, and pustules. After local anesthesia, a 4 mm punch biopsy specimen was taken of an edematous, erythematous papule in each patient and from normal facial skin of volunteers with rosacea in similar locations. Skin samples were immersed in 4% paraformaldehyde solution that contained O.3%pitricacid and fixed at 4° Cfor4 hours. The specimens were then rinsed overnight in phosphate-buffered saline. Frozen sections, 14 limin thickness, were cut and incubated with primary antibody (1:400 dilution) for 48 hours at 4° C. Later, the sections were reincubated with 1:80 dilution of tetramethyl rhodamine isothiocyanate-conjugated goat antirabbit antibody (Boehringer Mannheim) for 30 minutes at 37° C. Between different steps, the sections were rinsed in phosphate-buffered saline for 15 minutes. The antiserum was diluted in phosphate-buffered saline containing 0.3%TritonX-IOO. The antiserum against SP was obtained from Peninsula Laboratories, Belmont, New York.
Results. A blinded reading of the specimens showed that SP-immunoreactive nerves were increased considerably around the blood vessels in the papillary dermis in lesional skin as compared with normal skin. Discussion. Rosacea is a chronic inflammatory skin disease of unknown origin. Vascular dilation, which is a characteristic feature of the disease, has not been adequately explained. The affected skin shows a normal response to mediators such as acetylcholine and there is no evidence ofvascular instability after cooling ofthe skin?' 8 The association between rosacea and migraine seems to be evidence for a primary vascular disease. In addition, vessel malfunction that causes leakage and inflammation has been postulated in the origin of the disease. 8 SP l which has potent vasodilatory activity, could be involved in the vascular dilation of rosacea. We speculate that in a genetically predisposed person, SP released from cutaneous sensory neurons may give rise to vascular dilation and a perivascular inflammatory infiltrate that may be operative in the induction and/or maintenance of rosacea.
REFERENCES I. Naukkarinen A, NickolotfBJ, Farber EM. Quantification of cutaneous sensory nerves and their substance P content in psoriasis. J Invest DermatoI1989;92:126-9.
2. Farber EM, Lanigan SW, Boer J. The role of cutaneous sensory nerves in the maintenance of psoriasis. Int 1 Dermato11990;29:418-20. 3. Kiil'k9iioglu N,
