Galanin 3 receptor-deficient mice show no alteration in the oxazolone-induced contact dermatitis phenotype.
Allergic contact dermatitis (ACD) is an inflammatory skin disease induced by allergen exposure and characterized by erythema, oedema and immune cell infiltration. The sensory peptide galanin (GAL) and its three receptors (GAL1-3 ) are involved in regulating inflammation. As GAL and its receptors are expressed in human and murine skin and GAL expression is increased in oxazolone-induced contact allergy, it could play a role in dermatitis. As GAL reduces neurogenic plasma extravasation in the mouse skin via GAL3 activation, the role of GAL3 in the oxazolone-induced dermatitis model was explored. Following topical challenge with oxazolone, GAL3 gene-deficient mice showed a trend towards reduced ear thickness. Plasma extravasation and neutrophil infiltration increased considerably upon oxazolone challenge in both GAL3 knockout animals and wild-type controls without any observable effect of the gene deletion. We conclude that a lack of GAL3 does not influence oxazolone-induced ACD.
Department of Pharmacology and Pharmacotherapy, School of Medicine, János Szentágothai Research Centre, Molecular Pharmacology Research Team, University of Pécs, Pécs, Hungary.
Bálint
B
Botz
Department of Pediatrics, Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Paracelsus Medical University, Salzburg, Austria.
Susanne M
SM
Brunner
Department of Pharmacology and Pharmacotherapy, School of Medicine, János Szentágothai Research Centre, Molecular Pharmacology Research Team, University of Pécs, Pécs, Hungary.
Ágnes
Á
Kemény
Department of Pharmacology and Pharmacotherapy, School of Medicine, János Szentágothai Research Centre, Molecular Pharmacology Research Team, University of Pécs, Pécs, Hungary.
Erika
E
Pintér
Departments of Pharmacology and Anesthesia, Pain Management & Perioperative Medicine, Dalhousie University, Halifax, NS, Canada.
Jason J
JJ
McDougall
Department of Pediatrics, Laura Bassi Centre of Expertise-THERAPEP, Research Program for Receptor Biochemistry and Tumor Metabolism, Paracelsus Medical University, Salzburg, Austria.
Barbara
B
Kofler
Department of Pharmacology and Pharmacotherapy, School of Medicine, János Szentágothai Research Centre, Molecular Pharmacology Research Team, University of Pécs, Pécs, Hungary.|MTA-PTE NAP B Chronic Pain Research Group, Pécs, Hungary.
Zsuzsanna
Z
Helyes
D000818:Animals; D017449:Dermatitis, Allergic Contact / Q000209:etiology / Q000378:metabolism*; D004195:Disease Models, Animal; D051379:Mice; D010081:Oxazolone; D044093:Receptor, Galanin, Type 3 / Q000378:metabolism*
D044093:Receptor, Galanin, Type 3; D010081:Oxazolone
ear oedema; inflammation; myeloperoxidase; neuropeptide; plasma leakage