Abstract |
«Study of the role and mechanism of microneurotrofins in psoriasis»
Psoriasis is a chronic inflammatory autoimmune skin disease, with a strongly negative
effect on patients’ health, affecting 1-2 % of Caucasian population. The triggeging
factors of this disease are multicausative, with a significantly role for many genes and
stress factors affecting in a alterative way in different population, as well as an
important impact of environmental factors.
The histological appearance of psoriasis consists of 1) the named acanthosis,
representing the demarked prolonged epidermis in psoriasis lesions, b) the
parakeratosis, wich is defined as the thickening of the keratin layer in epidermis, with
an abnormal differentiation of keratinocytes, and to conclude c) an increased
angiogenesis and infiltration of inflammatory cells, such as neutrophils, CD4+ and
CD8+ T cells, and dendritics cells, contributing to the pathogenesis of the disease.
The neurosteroid dehydroepiadrosterone has been investigated widly in diseases
classified as immunological disorders, demonstrating strong neuroprotective and
immunomodulatory properties, even in skin disorders like atopic dermatitis. More
precisely in psoriasis, DHEA has not been researched systematically, although first
findings indicate low levels of this neurosteroid in patients with psoriasis. The
exogeneous administration of DHEA has not been beneficial as the neurosteroid can
be immediately converted into androgen and estrogen.
BNN27 is synthetic analogue of DHEA wich seems to conserve the beneficial of
DHEA in immunological disorders like in vivo model of multiple sclerosis and model
of inflammatory pain, without being further converted into estrogen or androgen.
Our study agrees with the previous one, demonstrating a dimitution of the
pathological key points of the psoriasis, due to the administration of BNN27. In
particular, we observed a reduction in the triggering of the immunological response,
as dendritic cells(CD11c+) and antigen-presenting cells(MHC II+), as well as a
decrease in wide range of T-cells subsets, as CD4+ and CD8+. As a result of this
impairment, we showed that even the product of this immunological response as
cytokines (IL-6, IL-17A) are decreased in the group administrated with BNN27,
establishing a anti-inflammatory role for the DHEA analogue.
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