title: Evidence for increased expression of eotaxin and monocyte chemotactic protein-4 in atopic dermatitis.
abstract: BACKGROUND
  Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with tissue eosinophilia and the activation of T lymphocytes. The novel eosinophil chemoattractants, eotaxin and monocyte chemotactic protein (MCP)-4, are up-regulated at sites of allergic inflammation, yet their contribution to the pathophysiologic mechanisms of AD remains to be determined.
  
  
  OBJECTIVE
  We sought to investigate the expression of eotaxin and MCP-4 in acute and chronic lesions from patients with AD and to determine their relationship to the numbers of resident inflammatory cells.
  
  
  METHODS
  With use of in situ hybridization, the expression of eotaxin and MCP-4 messenger RNA (mRNA) in skin biopsy specimens from patients with acute and chronic AD skin lesions was compared with that of uninvolved skin from these patients and skin from healthy volunteers.
  
  
  RESULTS
  There was a constitutive expression of eotaxin and MCP-4 mRNA in skin biopsy specimens from healthy subjects. Positive signal for chemokine mRNA was observed both within the epidermis and inflammatory cells (macrophages, eosinophils, and T cells) of the subepidermis in AD skin lesions. Within the subepithelium acute and chronic skin lesions exhibited a significant increase in the numbers of eotaxin and MCP-4 mRNA-positive cells compared with uninvolved skin (P <.01), whereas the numbers of eotaxin and MCP-4 mRNA-positive cells were significantly higher in chronic AD compared with acute AD skin lesions (P <.005, P <.001, respectively). Correlations were observed between the expression of eotaxin and MCP-4 mRNA and the presence of eosinophils and macrophages, respectively, in AD lesions (r(2) = 0.84, r(2) = 0.94).
  
  
  CONCLUSIONS
  There is an increased expression of eotaxin and MCP-4 in acute and chronic lesions, suggesting that these chemotactic factors play a major role in the pathophysiologic mechanisms of AD.
authors.affiliation: Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
authors.forename: R A
authors.initials: RA
authors.lastname: Taha
authors.forename: E M
authors.initials: EM
authors.lastname: Minshall
authors.forename: D Y
authors.initials: DY
authors.lastname: Leung
authors.forename: M
authors.initials: M
authors.lastname: Boguniewicz
authors.forename: A
authors.initials: A
authors.lastname: Luster
authors.forename: S
authors.initials: S
authors.lastname: Muro
authors.forename: M
authors.initials: M
authors.lastname: Toda
authors.forename: Q A
authors.initials: QA
authors.lastname: Hamid
mesh_terms: D001706:Biopsy; D054413:Chemokine CCL11; D018925:Chemokines / Q000235:genetics; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil / Q000235:genetics; D016207:Cytokines / Q000235:genetics*; D003876:Dermatitis, Atopic / Q000235:genetics* / Q000378:metabolism*; D006801:Humans; D018945:Monocyte Chemoattractant Proteins / Q000235:genetics*; D012333:RNA, Messenger / Q000378:metabolism; D012867:Skin / Q000473:pathology
chemical_list: C515456:CCL11 protein, human; C099677:CCL13 protein, human; D054413:Chemokine CCL11; D018925:Chemokines; D019742:Chemokines, CC; D002631:Chemotactic Factors, Eosinophil; D016207:Cytokines; D018945:Monocyte Chemoattractant Proteins; D012333:RNA, Messenger