title: Neurotensin serum levels and skin gene expression are increased in atopic dermatitis.
abstract: BACKGROUND
  Neurotensin (NT) participates in immune responses, but the mechanisms are not known. We have previously shown that NT augments the ability of corticotropin-releasing hormone (CRH) to increase mast-cell-dependent vascular permeability in rodents. We also showed that NT stimulates human mastcell release of vascular endothelial growth factor, and that CRH is increased in the serum of patients with atopic dermatitis (AD), an inflammatory skin condition involving mast cells.
  
  
  OBJECTIVE
  To measure serum levels of NT, and lesional skin expression of NT and the main NT receptor (NTR-1) in AD, and to compare it with skin expression in chronic urticaria (CU) and urticaria pigmentosa (UP).
  
  
  METHODS
  Serum NT was measured with a Milliplex microbead array. Skin NT and NTR-1 gene expression was determined with quantitative polymerase chain reaction. Immunohistochemistry was performed using a mouse monoclonal antibody for NT, and a rabbit polyclonal antibody for NTR-1. Mast cells were counterstained with Leder dye.
  
  
  RESULTS
  Neurotensin is significantly elevated in the serum of patients with AD compared with healthy controls (P = 0.0001). NT gene expression is also significantly increased in lesional skin of patients with AD compared with controls (P = 0.0194). Moreover, immunohistochemistry of AD lesions shows NT > NTR-1 staining of perivascular cells, many of which are identified as mast cells after staining with Leder dye. There was no statistically significant difference in NT and NTR-1 lesional skin gene expression in patients with either CU or UP.
  
  
  CONCLUSIONS
  These results suggest that interactions between NT and mast cells may occur and contribute to AD pathogenesis.
authors.affiliation: Molecular Immunopharmacology and Drug Discovery Laboratory, Department of Molecular Physiology and Pharmacology, Tufts University School of Medicine, Boston, MA, 02111, U.S.A; Allergy Clinical Research Center, Allergy Section, Attikon General Hospital, Athens University Medical School, Athens, 12462, Greece; Program in Pharmacology and Experimental Therapeutics, Sackler School of Graduate Biomedical Sciences, Tufts University, Boston, MA, 02111, U.S.A.
authors.forename: M
authors.initials: M
authors.lastname: Vasiadi
authors.forename: A P
authors.initials: AP
authors.lastname: Mondolfi
authors.forename: K-D
authors.initials: KD
authors.lastname: Alysandratos
authors.forename: A
authors.initials: A
authors.lastname: Therianou
authors.forename: A
authors.initials: A
authors.lastname: Katsarou-Katsari
authors.forename: T
authors.initials: T
authors.lastname: Petrakopoulou
authors.forename: A
authors.initials: A
authors.lastname: Theoharidis
authors.forename: A
authors.initials: A
authors.lastname: Miniati
authors.forename: T C
authors.initials: TC
authors.lastname: Theoharides
mesh_terms: D000328:Adult; D003876:Dermatitis, Atopic / Q000235:genetics / Q000378:metabolism*; D005260:Female; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008407:Mast Cells / Q000378:metabolism; D009496:Neurotensin / Q000235:genetics / Q000378:metabolism*; D060888:Real-Time Polymerase Chain Reaction; D018028:Receptors, Neurotensin / Q000235:genetics / Q000378:metabolism; D012867:Skin / Q000378:metabolism; D014581:Urticaria / Q000378:metabolism; D014582:Urticaria Pigmentosa / Q000378:metabolism
chemical_list: D018028:Receptors, Neurotensin; C114036:neurotensin type 1 receptor; D009496:Neurotensin