Decreased serum interleukin-17 and increased transforming growth factor–β levels in subjects with metabolic syndrome (Chennai Urban Rural Epidemiology Study–95)

Fetuin-A is a liver-synthesized protein that is secreted into serum. Transforming growth factor-β (TGF-β) is a polypeptide member of the TGF-β superfamily of cytokines. The purpose of this study is to evaluate the effects of lifestyle modification and metformin on fetuin-A and Transforming Growth Factor-ß (TGF- ß) in metabolic syndrome (MetS). Forty MetS subjects were randomly assigned to treatment with placebo (n=20) or metformin (n=20) in addition to lifestyle modification for 12 weeks. All 40 participants completed the study. After 12 weeks, both groups had significant reductions in weight, body mass index (BMI), waist circumference (WC), systolic blood pressure (SBP) and diastolic blood pressure (DBP) (all p<0.001). The placebo group also had significant improvement in fasting plasma glucose (FPG) and C-reactive protein (CRP) (p<0,001 ; p<0.05 respectively). Weight, BMI, WC, FPG, 2-hour postprandial glucose (2h-PPG), high density lipoprotein cholesterol (HDL-C), triglycerides (TG), fetuin-A and TGF- ß in the metformin group decreased significantly compared to the placebo group. Reduction of plasma fetuin-A was significantly associated with TG in the metformin group. Lifestyle modification and treatment with metformin for 12 weeks improved cardio-metabolic risk factors in MetS and reduced fetuin-A levels.

Download Full-text

Increased serum levels of interleukin-17 and transforming growth factor-β in patients with Graves’ disease

IOP Conference Series Earth and Environmental Science ◽

10.1088/1755-1315/125/1/012163 ◽

2018 ◽

Vol 125 ◽

pp. 012163

Author(s):

D Elvira ◽

E Nasrul ◽

Y Sofyan ◽

E Decroli ◽

E Darwin

Keyword(s):

Growth Factor ◽

Transforming Growth Factor ◽

Transforming Growth Factor Β ◽

Serum Levels ◽

Graves Disease ◽

Interleukin 17

Download Full-text

Transforming Growth Factor–β Signaling in T Cells Promotes Stabilization of Atherosclerotic Plaques Through an Interleukin-17–Dependent Pathway

Science Translational Medicine ◽

10.1126/scitranslmed.3006133 ◽

2013 ◽

Vol 5 (196) ◽

pp. 196ra100-196ra100 ◽

Cited By ~ 101

Author(s):

Anton Gisterå ◽

Anna-Karin L. Robertson ◽

John Andersson ◽

Daniel F. J. Ketelhuth ◽

Olga Ovchinnikova ◽

...

Keyword(s):

T Cells ◽

Smooth Muscle ◽

Growth Factor ◽

Transforming Growth Factor ◽

Smooth Muscle Actin ◽

Transforming Growth Factor Β ◽

Atherosclerotic Plaques ◽

Interleukin 17 ◽

Type I ◽

T Helper 17

Adaptive immunity has a major impact on atherosclerosis, with pro- and anti-atherosclerotic effects exerted by different subpopulations of T cells. Transforming growth factor–β (TGF-β) may promote development either of anti-atherosclerotic regulatory T cells or of T helper 17 (TH17) cells, depending on factors in the local milieu. We have addressed the effect on atherosclerosis of enhanced TGF-β signaling in T cells. Bone marrow from mice with a T cell–specific deletion ofSmad7, a potent inhibitor of TGF-β signaling, was transplanted into hypercholesterolemicLdlr−/−mice.Smad7-deficient mice had significantly larger atherosclerotic lesions that contained large collagen-rich caps, consistent with a more stable phenotype. The inflammatory cytokine interleukin-6 (IL-6) was expressed in the atherosclerotic aorta, and increased mRNA for IL-17A and the TH17-specific transcription factor RORγt were detected in draining lymph nodes. TreatingSmad7-deficient chimeras with neutralizing IL-17A antibodies reversed stable cap formation. IL-17A stimulated collagen production by human vascular smooth muscle cells, and RORγt mRNA correlated positively with collagen type I and α-smooth muscle actin mRNA in a biobank of human atherosclerotic plaques. These data link IL-17A to induction of a stable plaque phenotype, could lead to new plaque-stabilizing therapies, and should prompt an evaluation of cardiovascular events in patients treated with IL-17 receptor blockade.

Download Full-text