TY - JOUR
TI - Serum neurotensin (NT) is increased in psoriasis and NT induces vascular
endothelial growth factor release from human mast cells
AU - Vasiadi, M.
AU - Therianou, A.
AU - Alysandratos, K. D. and
AU - Katsarou-Katsari, A.
AU - Petrakopoulou, T.
AU - Theoharides, A. and
AU - Papadavid, E.
AU - Stavrianeas, N.
AU - Antoniou, C.
AU - Kalogeromitros,
AU - D.
AU - Theoharides, T. C.
JO - British Journal of Dermatology
PY - 2012
VL - 166
TODO - 6
SP - 1349-1352
PB - Wiley-Blackwell
SN - 0007-0963, 1365-2133
TODO - 10.1111/j.1365-2133.2012.10843.x
TODO - null
TODO - Background Psoriasis involves skin inflammation that often worsens with
stress, but the mechanism of this effect remains obscure. We have shown
that corticotropin-releasing hormone (CRH) is increased in the serum of
patients with psoriasis. A peptide, neurotensin (NT), can trigger skin
histamine release and augment the ability of CRH to increase skin
vascular permeability.
Objectives To investigate the serum level of NT, and the expression of
genes for NT and NT receptor-1 (NTR-1) in lesional and nonlesional skin
of patients with psoriasis, compared with normal controls. Also, to
study the effect of NT on human mast cell release of vascular
endothelial growth factor (VEGF), which is increased in psoriatic skin.
Methods Serum was obtained from patients with psoriasis (n = 56) and
controls (n = 33); NT levels were measured with the Milliplex microbead
assay. Biopsies were obtained from the lesional and nonlesional skin of
patients with chronic plaque psoriasis (n = 40), who had not received
any treatment for at least 15 days and were free of any systemic
inflammatory diseases. Control skin samples were obtained from healthy
subjects (n = 30). Expression of genes for NT and NTR-1 in the skin was
evaluated by quantitative reverse transcriptase-polymerase chain
reaction. LAD2 human mast cells were stimulated by NT (1 mu mol L-1) for
24 h and VEGF was measured by enzyme-linked immunosorbent assay.
Results Serum NT was increased in patients with psoriasis, while
expression of genes for NT and NTR-1 in lesional skin was decreased
compared with controls. NT induced VEGF release from mast cells and was
augmented by interleukin-33.
Conclusion NT may play a role in psoriasis pathogenesis and its
worsening by stress, at least in part through activation of skin mast
cells.
ER -