Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis

Walter Fries, Carmelo Muja, Carmela Crisafulli, Giuseppe Costantino, Giuseppe Longo, Salvatore Cuzzocrea, Emanuela Mazzon

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Loss of epithelial barrier integrity is considered an early step in the pathogenesis of Crohn's disease (CD), and the rate of enterocyte apoptosis is one of the determinants of the intestinal barrier function. Tumor necrosis factor-α (TNF-α), one of the major proinflammatory mediators in CD, is one of the extrinsic signals which initiate apoptosis of enterocytes. The aim of this study was to investigate the early effects of experimental colitis on enterocyte apoptosis, and the effects of two anti-TNF treatments, infliximab (IFX) and etanercept (ETC). In addition, the importance of receptor I for TNF was tested in TNFR-1 -/- mice. Circulating TNF-α levels were effectively reduced by IFX and ETC (p-/- animals. The anti-apoptotic protein Bcl-2 was expressed in the ileal epithelium under control conditions, but was suppressed in DNB-colitis. Expression of Bcl-2 was maintained in both anti-TNF treatments and TNFR-1 -/- mice. DNB colitis induced a very early, rapid increase of enterocyte apoptosis. Both anti-TNF strategies, IFX and ETC, were equally effective in suppressing enterocyte apoptosis, most likely by inactivation of circulating TNF-α.

Original languageEnglish
Pages (from-to)169-180
Number of pages12
JournalInternational Journal of Medical Sciences
Volume5
Issue number4
Publication statusPublished - Jul 3 2008

Fingerprint

Enterocytes
Colitis
Apoptosis
Tumor Necrosis Factor-alpha
Crohn Disease
Apoptosis Regulatory Proteins
Tumor Necrosis Factor Receptors
Epithelium
Etanercept
Infliximab

Keywords

  • Apoptosis
  • Enterocyte
  • Experimental colitis
  • TNF-α

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis. / Fries, Walter; Muja, Carmelo; Crisafulli, Carmela; Costantino, Giuseppe; Longo, Giuseppe; Cuzzocrea, Salvatore; Mazzon, Emanuela.

In: International Journal of Medical Sciences, Vol. 5, No. 4, 03.07.2008, p. 169-180.

Research output: Contribution to journalArticle

Fries, W, Muja, C, Crisafulli, C, Costantino, G, Longo, G, Cuzzocrea, S & Mazzon, E 2008, 'Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis', International Journal of Medical Sciences, vol. 5, no. 4, pp. 169-180.
Fries W, Muja C, Crisafulli C, Costantino G, Longo G, Cuzzocrea S et al. Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis. International Journal of Medical Sciences. 2008 Jul 3;5(4):169-180.
Fries, Walter ; Muja, Carmelo ; Crisafulli, Carmela ; Costantino, Giuseppe ; Longo, Giuseppe ; Cuzzocrea, Salvatore ; Mazzon, Emanuela. / Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis. In: International Journal of Medical Sciences. 2008 ; Vol. 5, No. 4. pp. 169-180.
@article{e6ad142274da4a23839502457a71f8ec,
title = "Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis",
abstract = "Loss of epithelial barrier integrity is considered an early step in the pathogenesis of Crohn's disease (CD), and the rate of enterocyte apoptosis is one of the determinants of the intestinal barrier function. Tumor necrosis factor-α (TNF-α), one of the major proinflammatory mediators in CD, is one of the extrinsic signals which initiate apoptosis of enterocytes. The aim of this study was to investigate the early effects of experimental colitis on enterocyte apoptosis, and the effects of two anti-TNF treatments, infliximab (IFX) and etanercept (ETC). In addition, the importance of receptor I for TNF was tested in TNFR-1 -/- mice. Circulating TNF-α levels were effectively reduced by IFX and ETC (p-/- animals. The anti-apoptotic protein Bcl-2 was expressed in the ileal epithelium under control conditions, but was suppressed in DNB-colitis. Expression of Bcl-2 was maintained in both anti-TNF treatments and TNFR-1 -/- mice. DNB colitis induced a very early, rapid increase of enterocyte apoptosis. Both anti-TNF strategies, IFX and ETC, were equally effective in suppressing enterocyte apoptosis, most likely by inactivation of circulating TNF-α.",
keywords = "Apoptosis, Enterocyte, Experimental colitis, TNF-α",
author = "Walter Fries and Carmelo Muja and Carmela Crisafulli and Giuseppe Costantino and Giuseppe Longo and Salvatore Cuzzocrea and Emanuela Mazzon",
year = "2008",
month = "7",
day = "3",
language = "English",
volume = "5",
pages = "169--180",
journal = "International Journal of Medical Sciences",
issn = "1449-1907",
publisher = "Ivyspring International Publisher",
number = "4",

}

TY - JOUR

T1 - Infliximab and etanercept are equally effective in reducing enterocyte apoptosis in experimental colitis

AU - Fries, Walter

AU - Muja, Carmelo

AU - Crisafulli, Carmela

AU - Costantino, Giuseppe

AU - Longo, Giuseppe

AU - Cuzzocrea, Salvatore

AU - Mazzon, Emanuela

PY - 2008/7/3

Y1 - 2008/7/3

N2 - Loss of epithelial barrier integrity is considered an early step in the pathogenesis of Crohn's disease (CD), and the rate of enterocyte apoptosis is one of the determinants of the intestinal barrier function. Tumor necrosis factor-α (TNF-α), one of the major proinflammatory mediators in CD, is one of the extrinsic signals which initiate apoptosis of enterocytes. The aim of this study was to investigate the early effects of experimental colitis on enterocyte apoptosis, and the effects of two anti-TNF treatments, infliximab (IFX) and etanercept (ETC). In addition, the importance of receptor I for TNF was tested in TNFR-1 -/- mice. Circulating TNF-α levels were effectively reduced by IFX and ETC (p-/- animals. The anti-apoptotic protein Bcl-2 was expressed in the ileal epithelium under control conditions, but was suppressed in DNB-colitis. Expression of Bcl-2 was maintained in both anti-TNF treatments and TNFR-1 -/- mice. DNB colitis induced a very early, rapid increase of enterocyte apoptosis. Both anti-TNF strategies, IFX and ETC, were equally effective in suppressing enterocyte apoptosis, most likely by inactivation of circulating TNF-α.

AB - Loss of epithelial barrier integrity is considered an early step in the pathogenesis of Crohn's disease (CD), and the rate of enterocyte apoptosis is one of the determinants of the intestinal barrier function. Tumor necrosis factor-α (TNF-α), one of the major proinflammatory mediators in CD, is one of the extrinsic signals which initiate apoptosis of enterocytes. The aim of this study was to investigate the early effects of experimental colitis on enterocyte apoptosis, and the effects of two anti-TNF treatments, infliximab (IFX) and etanercept (ETC). In addition, the importance of receptor I for TNF was tested in TNFR-1 -/- mice. Circulating TNF-α levels were effectively reduced by IFX and ETC (p-/- animals. The anti-apoptotic protein Bcl-2 was expressed in the ileal epithelium under control conditions, but was suppressed in DNB-colitis. Expression of Bcl-2 was maintained in both anti-TNF treatments and TNFR-1 -/- mice. DNB colitis induced a very early, rapid increase of enterocyte apoptosis. Both anti-TNF strategies, IFX and ETC, were equally effective in suppressing enterocyte apoptosis, most likely by inactivation of circulating TNF-α.

KW - Apoptosis

KW - Enterocyte

KW - Experimental colitis

KW - TNF-α

UR - http://www.scopus.com/inward/record.url?scp=47349097005&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=47349097005&partnerID=8YFLogxK

M3 - Article

VL - 5

SP - 169

EP - 180

JO - International Journal of Medical Sciences

JF - International Journal of Medical Sciences

SN - 1449-1907

IS - 4

ER -