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Chronic heart failure (CHF) is associated with elevated concentrations of tumor necrosis factor (TNF)  α  and cardiotrophin-1 (CT-1) and altered peripheral blood mononuclear cell (PBMC) function. Therefore, we tested whether CT-1 induces TNF α  in PBMC of healthy volunteers.  CT-1 induced in PBMC TNF α  protein in the supernatant and TNF α  mRNA in a concentration- and time-dependent manner determined by ELISA and real-time PCR, respectively. Maximal TNF α  protein was achieved with 100 ng/mL CT-1 after 3–6 hours and maximal TNF α  mRNA induction after 1 hour. ELISA data were confirmed using immunofluorescent flow cytometry. Inhibitor studies with actinomycin D and brefeldin A showed that both protein synthesis and intracellular transport are essential for CT-1 induced TNF α  expression. CT-1 caused a dose dependent nuclear factor (NF)  κ B translocation. Parthenolide inhibited both NF κ B translocation and TNF α  protein expression indicating that NF κ B seems to be necessary.  We revealed a new mechanism for elevated serum TNF α  concentrations and PBMC activation in CHF besides the hypothesis of PBMC activation by bacterial translocation from the gut.

Cardiotrophin-1 Induces Tumor Necrosis Factor Synthesis in Human Peripheral Blood Mononuclear Cells