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Multiplex Cytokine Profiling of Stimulated Mouse Splenocytes Using a Cytometric Bead-based Immunoassay Platform
Published on: November 9, 2017
[Cytokine networks and their endogenous modulators in patients with congestive heart failure]
1Department of Cardiology, Kunming General Hospital, Chengdu Military Area, Kunming 650032, China.
Insights
Cytokine network imbalance, with increased inflammatory markers like tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), is linked to severe congestive heart failure (CHF). This suggests a role in CHF development and progression.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Context:
- Congestive heart failure (CHF) is a complex syndrome with poorly understood pathophysiological mechanisms.
- Cytokines, key mediators of inflammation and immune response, are increasingly recognized for their role in cardiovascular diseases.
Purpose:
- To investigate the pathophysiological role of the cytokine network and its modulators in the development of congestive heart failure (CHF).
- To quantify plasma levels of specific cytokines and their receptors in CHF patients compared to healthy controls.
Summary:
- Patients with CHF exhibited elevated plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and soluble TNF receptor I (sTNF-RI), alongside decreased transforming growth factor-beta (TGF-beta).
- Ratios of TNF-alpha/sTNF-RI and TNF-alpha/TGF-beta were higher in CHF patients, particularly those with advanced heart failure (functional class IV).
- TNF-alpha levels positively correlated with IL-6 and sTNF-RI, and negatively with TGF-beta, indicating a pro-inflammatory cytokine shift.
Impact:
- The findings highlight a significant imbalance in the cytokine network in severe CHF, characterized by increased pro-inflammatory and inadequately regulated anti-inflammatory cytokines.
- This dysregulation of the cytokine network may be a critical factor in the development and progression of congestive heart failure.
- Understanding these cytokine interactions provides potential targets for novel therapeutic strategies in managing CHF.
Objective:
To explore the pathophysiological role of cytokine network and their endogenous modulators in the development of congestive heart failure (CHF).
Methods:
Plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-6(IL-6), soluble TNF receptor I (sTNF-RI) and transforming growth factor (TGF)-beta were measured by enzyme-linked immunoassay in 52 CHF patients with various degrees of heart failure and in 30 healthy controls.
Results:
Patients with CHF had increased plasma concentrations of TNF alpha, IL-6 and sTNF-RI, but decreased levels of TGF-beta. They also had elevated ratios of TNF-alpha/sTNF-RI and TNF-alpha/TGF-beta, particularly those in functional class IV. The levels of TNF-alpha were positively correlated with IL-6 and sTNF-RI but negatively correlated with TGF-beta(P < 0.01).
Conclusions:
The imbalance in the cytokine network were most pronounced in patients with the most severe heart failure. CHF may be accompanied by a shift toward enhanced levels of inflammatory cytokines combined with inadequately raised or even decreased levels of anti-inflammatory cytokines. A poorly regulated cytokine network may be involved in the development and progression of CHF.
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