Research article

Early inflammatory markers in elicitation of allergic contact dermatitis

Andrea Martín¹ , Norberto Gallino² , Julio Gagliardi² , Susana Ortiz³ , Alejandro Ruiz Lascano⁴ , Ana Diller⁵ , María Cristina Daraio² , Adrián Kahn² , Ana Lía Mariani^{* 6} and Horacio Marcelo Serra^{* 1}

¹Dpto. Bioquímica Clínica, Facultad de Ciencias Químicas – Universidad Nacional de Córdoba, Córdoba, Argentina

²Servicio de Alergia e Inmunología, Hospital Privado. Córdoba, Argentina

³Patología, Facultad de Ciencias Químicas – Universidad Nacional de Córdoba, Córdoba, Argentina

⁴Servicio de Dermatología, Hospital Privado, Córdoba, Argentina

⁵Patología, Hospital Privado, Córdoba, Argentina

⁶Universidad Nacional de Misiones (UNaM), Argentina

author email corresponding author email* Contributed equally

BMC Dermatology 2002, 2:9doi:10.1186/1471-5945-2-9

Published:	7 August 2002

Abstract

Background

Allergic Contact Dermatitis (ACD) is regarded as a T-cell-mediated delayed-type hypersensitivity reaction. We studied the kinetics of the expression of CS-1 fibronectin, thymus and activation-regulated chemokine (CCL17/ TARC) and different chemokine receptors (CR) in skin biopsies from individuals suffering from back problems, with the antigen responsible of their contact dermatitis and an irrelevant antigen.

Methods

Samples were taken at 2, 10, and 48 hours for histological and immunohistochemical studies using monoclonal antibodies against human CS-1 fibronectin, CCL17, CD3, CD68, CD49d, CXCR3, CCR5, and CCR3.

Results

At positive antigen stimulated sites there was an early expression of CS-1 fibronectin (2 hours), followed by CCL17 and a later accumulation of alplha4/beta1+ (CD49d), CD3+, CD68+, CXCR3+ and CCR5+ mononuclear cells. At 48 hours, approximately 59 % of infiltrating cells were CXCR3+, 42% CCR5+, and only 14 % CCR3+.

Conclusions

These results showed for the first time a very early expression of CS-1 fibronectin which preceded production of CCL17 in blood endothelial cells (BCEs) from patients' skin with ACD. The role of these molecules in recruitment of monocytes and effector T cells in ACD is discussed.