Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio.

Translated title of the contribution: Activation and role of the tumor necrosis factor-alpha in congestive heart failure

T. Bachetti, L. Comini, L. Agnoletti, G. Gaia, B. Milanesi, S. Curello, A. Corti, R. Ferrari, O. Visioli

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Recently, an activation of the immune system has been demonstrated in congestive heart failure (CHF). Aim of this study was to evaluate the effects of CHF on the activation of alpha tumor necrosis factor (TNF-alpha), a pleiotropic cytokine. Since the soluble forms of the TNF membrane receptors, sTNF-RI and sTNF-RII, have been shown to modulate TNF-alpha biological activity, we determined antigenic TNF-alpha, bioactive TNF-alpha, sTNF-RI and sTNF-RII in 52 patients with varying degrees of CHF (NYHA functional class II, III, IV). The etiology of CHF was coronary artery disease in 51% of the patients, idiopathic dilated cardiomyopathy in 38% and valvular disease in 11%. All patients were treated with ACE-inhibitors, digoxin and inotropic agents. Antigenic TNF-alpha was significantly increased in NYHA functional class IV patients (from 12.1 +/- 7.6 to 38.5 +/- 12.4 pg/ml, p <0.001) whereas cytotoxic activity was always under the detection limit of the assay (100 pg/ml). Soluble TNF receptors were significantly elevated in NYHA functional class IV patients: sTNF-RI increased from 1.27 +/- 0.48 to 4.54 +/- 2.11 ng/ml (p <0.001) and sTNF-RII from 2.25 +/- 0.55 to 7.78 +/- 2.13 ng/ml (p <0.001). The possible modulation of TNF-alpha biological activity by the soluble receptors was investigated by means of spiking experiments after addition of 625 pg/ml human recombinant TNF-alpha to each serum sample. The biological activity of the added TNF-alpha was significantly inhibited by the high levels of soluble receptors present in the sera of NYHA functional class IV patients (from 625 to 249 +/- 176 pg/ml, p <0.001). The results show that TNF-alpha and its soluble receptors are activated in severe CHF. The high concentration of soluble TNF receptors circulating in CHF patients are likely to play a protective role against TNF-alpha biological activity.

Original languageItalian
Pages (from-to)343-347
Number of pages5
JournalCardiologia
Volume41
Issue number4
Publication statusPublished - Apr 1996

Fingerprint

Heart Failure
Tumor Necrosis Factor-alpha
Tumor Necrosis Factor Receptors
Digoxin
Dilated Cardiomyopathy
Serum
Angiotensin-Converting Enzyme Inhibitors
Limit of Detection
Coronary Artery Disease
Immune System
Cytokines
Membranes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Bachetti, T., Comini, L., Agnoletti, L., Gaia, G., Milanesi, B., Curello, S., ... Visioli, O. (1996). Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio. Cardiologia, 41(4), 343-347.

Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio. / Bachetti, T.; Comini, L.; Agnoletti, L.; Gaia, G.; Milanesi, B.; Curello, S.; Corti, A.; Ferrari, R.; Visioli, O.

In: Cardiologia, Vol. 41, No. 4, 04.1996, p. 343-347.

Research output: Contribution to journalArticle

Bachetti, T, Comini, L, Agnoletti, L, Gaia, G, Milanesi, B, Curello, S, Corti, A, Ferrari, R & Visioli, O 1996, 'Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio.', Cardiologia, vol. 41, no. 4, pp. 343-347.
Bachetti, T. ; Comini, L. ; Agnoletti, L. ; Gaia, G. ; Milanesi, B. ; Curello, S. ; Corti, A. ; Ferrari, R. ; Visioli, O. / Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio. In: Cardiologia. 1996 ; Vol. 41, No. 4. pp. 343-347.
@article{10cd8eae09c34e2a834f27baa5ddae8c,
title = "Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio.",
abstract = "Recently, an activation of the immune system has been demonstrated in congestive heart failure (CHF). Aim of this study was to evaluate the effects of CHF on the activation of alpha tumor necrosis factor (TNF-alpha), a pleiotropic cytokine. Since the soluble forms of the TNF membrane receptors, sTNF-RI and sTNF-RII, have been shown to modulate TNF-alpha biological activity, we determined antigenic TNF-alpha, bioactive TNF-alpha, sTNF-RI and sTNF-RII in 52 patients with varying degrees of CHF (NYHA functional class II, III, IV). The etiology of CHF was coronary artery disease in 51{\%} of the patients, idiopathic dilated cardiomyopathy in 38{\%} and valvular disease in 11{\%}. All patients were treated with ACE-inhibitors, digoxin and inotropic agents. Antigenic TNF-alpha was significantly increased in NYHA functional class IV patients (from 12.1 +/- 7.6 to 38.5 +/- 12.4 pg/ml, p <0.001) whereas cytotoxic activity was always under the detection limit of the assay (100 pg/ml). Soluble TNF receptors were significantly elevated in NYHA functional class IV patients: sTNF-RI increased from 1.27 +/- 0.48 to 4.54 +/- 2.11 ng/ml (p <0.001) and sTNF-RII from 2.25 +/- 0.55 to 7.78 +/- 2.13 ng/ml (p <0.001). The possible modulation of TNF-alpha biological activity by the soluble receptors was investigated by means of spiking experiments after addition of 625 pg/ml human recombinant TNF-alpha to each serum sample. The biological activity of the added TNF-alpha was significantly inhibited by the high levels of soluble receptors present in the sera of NYHA functional class IV patients (from 625 to 249 +/- 176 pg/ml, p <0.001). The results show that TNF-alpha and its soluble receptors are activated in severe CHF. The high concentration of soluble TNF receptors circulating in CHF patients are likely to play a protective role against TNF-alpha biological activity.",
author = "T. Bachetti and L. Comini and L. Agnoletti and G. Gaia and B. Milanesi and S. Curello and A. Corti and R. Ferrari and O. Visioli",
year = "1996",
month = "4",
language = "Italian",
volume = "41",
pages = "343--347",
journal = "Cardiologia (Rome, Italy)",
issn = "0393-1978",
publisher = "Societa Italiana di Cardiologia",
number = "4",

}

TY - JOUR

T1 - Attivazione e ruolo del fattore di necrosi tumorale alfa nello scompenso cardiaco congestizio.

AU - Bachetti, T.

AU - Comini, L.

AU - Agnoletti, L.

AU - Gaia, G.

AU - Milanesi, B.

AU - Curello, S.

AU - Corti, A.

AU - Ferrari, R.

AU - Visioli, O.

PY - 1996/4

Y1 - 1996/4

N2 - Recently, an activation of the immune system has been demonstrated in congestive heart failure (CHF). Aim of this study was to evaluate the effects of CHF on the activation of alpha tumor necrosis factor (TNF-alpha), a pleiotropic cytokine. Since the soluble forms of the TNF membrane receptors, sTNF-RI and sTNF-RII, have been shown to modulate TNF-alpha biological activity, we determined antigenic TNF-alpha, bioactive TNF-alpha, sTNF-RI and sTNF-RII in 52 patients with varying degrees of CHF (NYHA functional class II, III, IV). The etiology of CHF was coronary artery disease in 51% of the patients, idiopathic dilated cardiomyopathy in 38% and valvular disease in 11%. All patients were treated with ACE-inhibitors, digoxin and inotropic agents. Antigenic TNF-alpha was significantly increased in NYHA functional class IV patients (from 12.1 +/- 7.6 to 38.5 +/- 12.4 pg/ml, p <0.001) whereas cytotoxic activity was always under the detection limit of the assay (100 pg/ml). Soluble TNF receptors were significantly elevated in NYHA functional class IV patients: sTNF-RI increased from 1.27 +/- 0.48 to 4.54 +/- 2.11 ng/ml (p <0.001) and sTNF-RII from 2.25 +/- 0.55 to 7.78 +/- 2.13 ng/ml (p <0.001). The possible modulation of TNF-alpha biological activity by the soluble receptors was investigated by means of spiking experiments after addition of 625 pg/ml human recombinant TNF-alpha to each serum sample. The biological activity of the added TNF-alpha was significantly inhibited by the high levels of soluble receptors present in the sera of NYHA functional class IV patients (from 625 to 249 +/- 176 pg/ml, p <0.001). The results show that TNF-alpha and its soluble receptors are activated in severe CHF. The high concentration of soluble TNF receptors circulating in CHF patients are likely to play a protective role against TNF-alpha biological activity.

AB - Recently, an activation of the immune system has been demonstrated in congestive heart failure (CHF). Aim of this study was to evaluate the effects of CHF on the activation of alpha tumor necrosis factor (TNF-alpha), a pleiotropic cytokine. Since the soluble forms of the TNF membrane receptors, sTNF-RI and sTNF-RII, have been shown to modulate TNF-alpha biological activity, we determined antigenic TNF-alpha, bioactive TNF-alpha, sTNF-RI and sTNF-RII in 52 patients with varying degrees of CHF (NYHA functional class II, III, IV). The etiology of CHF was coronary artery disease in 51% of the patients, idiopathic dilated cardiomyopathy in 38% and valvular disease in 11%. All patients were treated with ACE-inhibitors, digoxin and inotropic agents. Antigenic TNF-alpha was significantly increased in NYHA functional class IV patients (from 12.1 +/- 7.6 to 38.5 +/- 12.4 pg/ml, p <0.001) whereas cytotoxic activity was always under the detection limit of the assay (100 pg/ml). Soluble TNF receptors were significantly elevated in NYHA functional class IV patients: sTNF-RI increased from 1.27 +/- 0.48 to 4.54 +/- 2.11 ng/ml (p <0.001) and sTNF-RII from 2.25 +/- 0.55 to 7.78 +/- 2.13 ng/ml (p <0.001). The possible modulation of TNF-alpha biological activity by the soluble receptors was investigated by means of spiking experiments after addition of 625 pg/ml human recombinant TNF-alpha to each serum sample. The biological activity of the added TNF-alpha was significantly inhibited by the high levels of soluble receptors present in the sera of NYHA functional class IV patients (from 625 to 249 +/- 176 pg/ml, p <0.001). The results show that TNF-alpha and its soluble receptors are activated in severe CHF. The high concentration of soluble TNF receptors circulating in CHF patients are likely to play a protective role against TNF-alpha biological activity.

UR - http://www.scopus.com/inward/record.url?scp=0030116255&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030116255&partnerID=8YFLogxK

M3 - Articolo

C2 - 8674103

AN - SCOPUS:0030116255

VL - 41

SP - 343

EP - 347

JO - Cardiologia (Rome, Italy)

JF - Cardiologia (Rome, Italy)

SN - 0393-1978

IS - 4

ER -