10.6084/m9.figshare.4702597.v1
Roth S.
Roth
S.
Spalinger M.R.
Spalinger
M.R.
Müller I.
Müller
I.
Lang S.
Lang
S.
Rogler G.
Rogler
G.
Scharl M.
Scharl
M.
Supplementary Material for: Bilberry-Derived Anthocyanins Prevent IFN-γ-Induced Pro-Inflammatory Signalling and Cytokine Secretion in Human THP-1 Monocytic Cells
Karger Publishers
2017
Anthocyanins
TNF-α
NF-κB
JAK/STA
Inflammator bowel disease
2017-02-28 14:25:28
Dataset
https://karger.figshare.com/articles/dataset/Supplementary_Material_for_Bilberry-Derived_Anthocyanins_Prevent_IFN-_-Induced_Pro-Inflammatory_Signalling_and_Cytokine_Secretion_in_Human_THP-1_Monocytic_Cells/4702597
<p><b><i>Background/Aims:</i></b> Anthocyanins are plant-derived dietary
components that are highly abundant, for example, in bilberries. We
have previously demonstrated that anthocyanins exert anti-inflammatory
properties in mouse colitis models and ameliorate disease activity in
ulcerative colitis patients. Here, we studied the molecular mechanisms
through which anthocyanin-containing bilberry extract (BE) exerts
anti-inflammatory effects in human monocytic THP-1 cells. <b><i>Methods:</i></b>
THP-1 cells were pre-incubated with BE 20 min prior to TNF-a or IFN-γ
(100 ng/ml each) stimulation. Signalling protein activation was studied
by Western blotting, mRNA expression by quantitative PCR and cytokine
secretion by ELISA. <b><i>Results:</i></b> IFN-γ-induced phosphorylation
of STAT1 and STAT3 was significantly reduced by BE co-treatment.
Consequently, levels of mRNA expression and/or cytokine secretion of
MCP-1, IL-6, TNF-a, ICAM-1, and T-bet were lower with BE co-treatment.
In contrast, BE enhanced TNF-a-mediated p65-NF-γB phosphorylation but
reduced ERK1/2 phosphorylation. BE co-treatment further increased
TNF-a-induced mRNA expression and secretion of NF-γB target genes, such
as IL-6, IL-8, and MCP-1, while mRNA levels of ICAM-1 were reduced. <b><i>Conclusions:</i></b>
BE co-treatment reduced IFN-γ-induced signal protein activation,
pro-inflammatory gene expression, and cytokine secretion, whereas it
enhanced TNF-a-induced responses. These findings suggest a distinct role
for anthocyanins in modulating inflammatory responses that need to be
further studied to fully understand anthocyanin-mediated effects.</p>