title: TARC and RANTES, but not CTACK, are induced in two models of allergic contact dermatitis. Effects of cilomilast and diflorasone diacetate on T-cell-attracting chemokines.
abstract: BACKGROUND
  Skin-infiltrating T cells play a predominant role in allergic and inflammatory skin diseases such as atopic dermatitis and allergic contact dermatitis. These T cells are attracted by chemotactic factors, e.g. RANTES (regulation on activation, normal T cell expressed and secreted; CCL5), TARC (thymus and activation regulated chemokine; CCL17) and CTACK (cutaneous T-cell attracting chemokine; CCL27).
  
  
  OBJECTIVE
  To investigate which T-cell-attracting chemokines are involved in allergic contact dermatitis in mice.
  
  
  METHODS
  Allergic contact dermatitis was induced by application of dinitrochlorobenzene (DNCB) or toluene-2,4-diisocyanate (TDI), and chemokine concentrations were determined by enzyme-linked immunosorbent assay. The effects on chemokine concentrations of the highly selective phosphodiesterase 4 inhibitor cilomilast and the glucocorticoid diflorasone diacetate were studied in mouse ears.
  
  
  RESULTS
  RANTES and TARC were elevated in both models of allergic contact dermatitis 24 h after challenge, whereas CTACK remained unchanged. The increase in RANTES was diminished in mouse ears pretreated with cilomilast or diflorasone diacetate. TARC was reduced by diflorasone diacetate in the DNCB model but was highly induced in the TDI model; in contrast, TARC was not influenced by cilomilast.
  
  
  CONCLUSIONS
  TARC and RANTES, but not CTACK, are involved in these two models of allergic contact dermatitis.
authors.affiliation: Department of Pharmacology, Toxicology and Pharmacy, School of Veterinary Medicine, Buenteweg 17, 30559 Hannover, Germany. wolfgang.baeumer@tiho-hannover.de
authors.forename: W
authors.initials: W
authors.lastname: Bäumer
authors.forename: U
authors.initials: U
authors.lastname: Seegers
authors.forename: M
authors.initials: M
authors.lastname: Braun
authors.forename: T
authors.initials: T
authors.lastname: Tschernig
authors.forename: M
authors.initials: M
authors.lastname: Kietzmann
mesh_terms: D000818:Animals; D001623:Betamethasone / Q000031:analogs & derivatives* / Q000494:pharmacology; D001993:Bronchodilator Agents / Q000494:pharmacology; D002264:Carboxylic Acids; D054414:Chemokine CCL17; D054425:Chemokine CCL27; D018946:Chemokine CCL5 / Q000378:metabolism*; D018925:Chemokines / Q000276:immunology*; D019742:Chemokines, CC / Q000378:metabolism*; D003509:Cyclohexanecarboxylic Acids; D017449:Dermatitis, Allergic Contact / Q000209:etiology / Q000276:immunology* / Q000517:prevention & control; D004195:Disease Models, Animal; D005260:Female; D007124:Immunoenzyme Techniques; D051379:Mice; D008807:Mice, Inbred BALB C; D009570:Nitriles; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology*
chemical_list: D001993:Bronchodilator Agents; D002264:Carboxylic Acids; C499538:Ccl17 protein, mouse; C119538:Ccl27a protein, mouse; D054414:Chemokine CCL17; D054425:Chemokine CCL27; D018946:Chemokine CCL5; D018925:Chemokines; D019742:Chemokines, CC; D003509:Cyclohexanecarboxylic Acids; D009570:Nitriles; C433247:Cilomilast; D001623:Betamethasone; C014477:diflorasone