Up-regulation of the chemokine CCL21 in the skin of subjects exposed to irritants

被引：37

作者：

Eberhard Y. ^{[1
]}

Ortiz S. ^{[2
]}

Ruiz Lascano A. ^{[3
]}

Kuznitzky R. ^{[3
]}

Serra H.M. ^{[1
]}

机构：

[1] Department of Immunology, School of Chemical Science, National University of Cordoba, Cordoba

[2] Department of Pathological Anatomy, School of Chemical Science, National University of Cordoba, Cordoba

[3] Clinic of Dermatology, Hospital Privado Cordoba, Cordoba

来源：

BMC Immunology | / 5卷 / 1期

关键词：

Sodium Lauryl Sulphate; Allergic Contact Dermatitis; Lymphatic Endothelial Cell; Inflammatory Skin Disease; High Endothelial Venule;

D O I：

10.1186/1471-2172-5-7

中图分类号：

学科分类号：

摘要：

Background: Expression of murine CCL21 by dermal lymphatic endothelial cells (LEC) has been demonstrated to be one of the most important steps in Langerhans cell emigration from skin. Previously, our group and others have found that this chemokine is up-regulated in different human inflammatory skin diseases mediated by diverse specific immune responses. This study was carried out to investigate the involvement of CCL21 in human skin after challenge with irritant agents responsible for inducing Irritant Contact Dermatitis (ICD). Results: Eleven normal individuals were challenged with different chemical or physical irritants. Two patients with Allergic Contact Dermatitis (ACD) were also challenged with the relevant antigen in order to have a positive control for CCL21 expression. Macroscopic as well as microscopic responses were evaluated. We observed typical ICD responses with mostly mononuclear cells in perivascular areas, but a predominance of polymorphonuclear cells away from the inflamed blood vessels and in the epidermis at 24 hours. Immunohistochemical studies showed up-regulation of CCL21 by lymphatic endothelial cells in all the biopsies taken from ICD and ACD lesions compared to normal skin. Kinetic study at 10, 48, 96 and 168 hours after contact with a classical irritant (sodium lauryl sulphate) showed that the expression of CCL21 was increased in lymphatic vessels at 10 hours, peaked at 48 hours, and then gradually declined. There was a strong correlation between CCL21 expression and the macroscopic response (r = 0.69; p = 0.0008), but not between CCL21 and the number of infiltrating cells in the lesions. Conclusions: These results provide new evidence for the role of CCL21 in inflammatory processes. Since the up-regulation of this chemokine was observed in ICD and ACD, it is tempting to speculate that this mechanism operates independently of the type of dermal insult, facilitating the emigration of CCR7+ cells. © 2004 Eberhard et al; licensee BioMed Central Ltd.

引用

共 35 条

[11]

D'Ambrosio D., Panina-Bordignon P., Sinigaglia F., Chemokine receptors in inflammation: An overview, J. Immunol. Methods, 273, pp. 3-13, (2003)

[12]

Engeman T.M., Gorbachev A.V., Gladue R.P., Heeger P.S., Fairchild R.L., Inhibition of functional T cell priming and contact hypersensitivity responses by treatment with anti-secondary lymphoid chemokine antibody during hapten sensitization, J. Immunol., 164, pp. 5207-5214, (2000)

[13]

Weninger W., Carlsen H.S., Goodarzi M., Moazed F., Crowley M.A., Baekkevold E.S., Cavanagh L.L., von Andrian U.H., Naive T cell recruitment to non-lymphoid tissues: A role for endothelium-expressed CC chemokine ligand 21 in autoimmune disease and lymphoid neogenesis, J. Immunol., 170, pp. 4638-4648, (2003)

[14]

Serra H.M., Eberhard Y., Martin A.P., Gallino N., Gagliardi J., Baena-Cagnani C.E., Ruiz Lascano A., Ortiz S., Mariani A.L., Uguccioni M., Secondary Lymphoid Tissue Chemokine (CCL21) is Up Regulated in Allergic Contact Dermatitis, Int. Arch. Allergy Immunol., 133, 1, pp. 64-71, (2004)

[15]

Katou F., Ohtani H., Nakayama T., Nagura H., Yoshie O., Motegi K., Differential expression of CCL19 by DC-Lamp+ mature dendritic cells in human lymph node versus chronically inflamed skin, J. Pathol., 199, 1, pp. 98-106, (2003)

[16]

Brasch J., Burgard J., Sterry W., Common pathogenetic pathways in allergic and irritant contact dermatitis, J. Invest. Dermatol., 98, pp. 166-170, (1992)

[17]

Martin A.P., Gagliardi J., Baena-Cagnani C.E., Eberhard Y., Uguccioni M., Gallino N., Mariani A.L., Serra H.M., Expression of CS-1 fibronectin precedes monocyte chemoattractant protein-1 production during elicitation of allergic contact dermatitis, Clin. Exp. Allergy, 33, pp. 1118-1124, (2003)

[18]

Corsini E., Galli C.L., Cytokines and irritant contact dermatitis, Toxicology Letters, 102-103, pp. 277-282, (1998)

[19]

Krasteva M., Kehren J., Ducluzeau M.T., Sayag M., Cacciapuoti M., Akiba H., Descotes J., Nicolas J.F., Contact dermatitis I. Pathophysiology of contact sensitivity, Eur. J. Dermatol., 9, 1, pp. 65-77, (1999)

[20]

Hedrick J.A., Zlotnik A., Identification and characterization of a novel b chemokine containing six conserved cysteines, J. Immunol., 159, pp. 1589-1593, (1997)

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