Analysis of the influence of adalimumab to the expression pattern of mRNA and protein of TGF-ß1-3 in dermal fibroblast exposed to lipopolysaccharide.
Postepy Dermatol Alergol
; 38(4): 597-602, 2021 Aug.
Article
em En
| MEDLINE
| ID: mdl-34658700
ABSTRACT
INTRODUCTION:
Psoriasis is a inflammatory illness, where incorrect expression of cytokines and bacteria lipopolysaccharide are observed. In the therapy of moderate to severe psoriasis anti-TNF drugs, i.e. adalimumab are used which have the influence for secreting another cytokines, such as transforming growth factor-ß (TGF-ß).AIM:
To analyse the expression profile of mRNA TGF-ß1-3 and proteins (TGF-ß1 and TGF-ß2) it codes in normal human dermal fibroblasts (NHDF) exposed to bacterial lipopolysaccharide (induction of inflammation) and adalimumab (anti-TNF drug). MATERIAL ANDMETHODS:
NHDFs treated with bacterial lipopolysaccharide at a medium concentration of 1 µg/ml for 8 h, and then added to an adalimumab culture at a concentration of 8 µg/ml and continued exposure of the fibroblasts to it for 2, 8 and 24 h. The molecular analysis included microarray, RTqPCR and ELISA assays.RESULTS:
Treating the skin fibroblast cells with LPS resulted in significant statistical changes in the expression of TGF-ß1 (↑) and TGF-ß2 (↓) in comparison to the control culture. Likewise, after adding adalimumab to the culture of NHDF treated previously with LPS, significant changes in the expression of TGF-ß1 (↑) and TGF-ß2 (↓) were noted in comparison to the control culture (p < 0.05). On the protein level it can be determined that LPS and adalimumab cause an increase in the concentration of TGF-ß1 and a decrease in the expression of TGF-ß2 in comparison to the control culture.CONCLUSIONS:
Blocking the signalling dependant on TNF-α using adalimumab causes an increase in the expression of TGF-ß1 and a simultaneous decrease in the case of TGF-ß2.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Postepy Dermatol Alergol
Ano de publicação:
2021
Tipo de documento:
Article