Aim
To analyse the expression profile of mRNA TGF-β1-3 and proteins (TGF-β1 and TGF-β2) it codes in normal human dermal fibroblasts (NHDF) exposed to bacterial lipopolysaccharide (induction of inflammation) and adalimumab (anti-TNF drug). Material and
Conclusions
Blocking the signalling dependant on TNF-α using adalimumab causes an increase in the expression of TGF-β1 and a simultaneous decrease in the case of TGF-β2.
Material and methods
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.
Methods
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-β1 (↑) and TGF-β2 (↓) 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-β1 (↑) and TGF-β2 (↓) 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-β1 and a decrease in the expression of TGF-β2 in comparison to the control culture. Conclusions: Blocking the signalling dependant on TNF-α using adalimumab causes an increase in the expression of TGF-β1 and a simultaneous decrease in the case of TGF-β2.