The TNF-alpha system in heart failure and after heart transplantation: plasma protein levels, mRNA expression, soluble receptors and plasma buffer capacity
Summary
This summary is machine-generated.In heart failure and after transplantation, elevated soluble tumour necrosis factor (sTNF) receptors increase TNF-alpha binding capacity. This suggests a potential mechanism for immunosuppression in these patients, despite normal TNF-alpha mRNA and plasma levels.
Area Of Science
- Cardiology
- Immunology
- Biochemistry
Background
- Tumour necrosis factor-alpha (TNF-alpha) is a cytokine with cardiodepressant properties.
- The TNF-alpha system is dysregulated in heart failure and post-heart transplantation, characterized by elevated soluble TNF receptors (sTNF-R1, sTNF-R2).
- These receptors bind TNF-alpha, influencing its bioavailability.
Purpose Of The Study
- To investigate the activity of the TNF-alpha system in patients experiencing heart failure.
- To assess the TNF-alpha system's activity in individuals following heart transplantation.
Main Methods
- Quantification of TNF-alpha mRNA expression in peripheral blood mononuclear cells via polymerase chain reaction.
- Measurement of plasma levels of TNF-alpha and soluble TNF receptors (sTNF-R1, sTNF-R2) using ELISA.
- Assessment of TNF-alpha binding capacity by measuring the buffer capacity of patient plasma.
Main Results
- TNF-alpha mRNA expression and plasma levels were comparable between patients and controls.
- Significantly elevated levels of soluble TNF receptors (sTNF-R1, sTNF-R2) were observed in patients (P <0.001).
- Increased TNF-alpha binding capacity in patient plasma led to decreased TNF-alpha recovery (P <0.05), with strong correlations between sTNF receptors and serum creatinine.
Conclusions
- The peripheral TNF-alpha system is not activated in heart failure and post-transplant patients, as indicated by mRNA and plasma levels.
- Elevated sTNF receptor levels enhance TNF-alpha binding capacity, reducing TNF-alpha bioavailability.
- This altered TNF-alpha system may contribute to an immunosuppressed state in these patient populations.
View abstract on PubMed