title: Role of substance P in an NC/Nga mouse model of atopic dermatitis-like disease.
abstract: BACKGROUND
  Atopic dermatitis (AD) can be exacerbated or induced in genetically predisposed individuals by psychological stress, which causes the release of substance P (SP). Therefore, SP may play an etiological role in the mechanisms underlying AD.
  
  
  METHODS
  Changes in the number of mast cells and SP-containing mast cells in lesional skin, and the serum concentrations of SP and IgE during the development of AD-like disease up to 8 weeks after the start of picryl chloride (PiCl) induction in NC/Nga mice were examined.
  
  
  RESULTS
  Clinical signs and symptoms seen in PiCl-treated NC/Nga mice as a model of AD-like disease began with erythema and haemorrhage, followed by oedema, superficial erosion, deep excoriation, scaling and dryness of the skin, as well as retarded growth, and the changes were exacerbated with an increase in the number of PiCl applications. An increase in the number of mast cells and eosinophil infiltration was observed in the lesional skin. The increase in SP-positive mast cells in the dermis in this model was significant from 1 week after the start of induction treatment, compared with intact mice, and SP-positive nerve fibres were observed in the dermis.
  
  
  CONCLUSIONS
  SP is a crucial mediator of both dermatitis and scratching behaviour in this model.
authors.affiliation: Department of Pharmacology, Kawanishi Pharma Research Institute, Nippon Boehringer Ingelheim Co. Ltd., Kawanishi, Japan. ohmura@boehringer-ingelheim.co.jp
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Ohmura
authors.forename: Ichiro
authors.initials: I
authors.lastname: Tsunenari
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Hayashi
authors.forename: Yayoi
authors.initials: Y
authors.lastname: Satoh
authors.forename: Ayako
authors.initials: A
authors.lastname: Konomi
authors.forename: Hirotoshi
authors.initials: H
authors.lastname: Nanri
authors.forename: Mamoru
authors.initials: M
authors.lastname: Kawachi
authors.forename: Makoto
authors.initials: M
authors.lastname: Morikawa
authors.forename: Toshihito
authors.initials: T
authors.lastname: Kadota
authors.forename: Hisashi
authors.initials: H
authors.lastname: Satoh
mesh_terms: D000818:Animals; D003876:Dermatitis, Atopic / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D004804:Eosinophils / Q000276:immunology; D007073:Immunoglobulin E / Q000097:blood; D007150:Immunohistochemistry; D015847:Interleukin-4 / Q000097:blood; D008297:Male; D008407:Mast Cells / Q000276:immunology; D051379:Mice; D010853:Picryl Chloride; D018709:Statistics, Nonparametric; D013373:Substance P / Q000097:blood / Q000276:immunology*
chemical_list: D015847:Interleukin-4; D013373:Substance P; D007073:Immunoglobulin E; D010853:Picryl Chloride