Abstracts DGKCH

IF 1.7 Q2 SURGERY Innovative Surgical Sciences Pub Date : 2024-04-01 DOI:10.1515/iss-2024-2005

Nariman Mokhaberi, Michalis Aftzoglou, Philipp Schneider, Daniel Biermann, Rainer Gerhard Kozlik-Feldmann, Christian Tomuschat, Christine Drießler, Armin-Johannes Michel, Andrea Schmedding, Florentine Weise, Niklas Dressler, N. Peukert, Johannes Düß, S. Mayer, M. Lacher, Jan Riedel, Yuqing Lu, Julia Elrod, S. Turial, Maciej Pech, Volker Aumann, A. Nyiredi, Lena Bode, Jan-Hendrik Gosemann, Gabriel Götz, Robin Wachowiak, Peter Zimmermann, Tomasz Baranski, Matthias Nissen, Ralf-Bodo Tröbs, I. Martynov, Monika Sparber-Sauer, Amadeus T Heinz, C. Vokuhl, Martin Ebinger, J. Gesche, Marc Münter, E. Koscielniak, Jörg Fuchs, Guido Seitz, Mark Schneider, Ruben Visschers, U. Kontny, Ulf Neumann, Wilhelmus van Gemert

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Abstract

Impaired intestinal endotoxin tolerance is seen in human preterms suffering from necrotizing enterocolitis (NEC), but the underlying mechanism remains unknown. Activation of the TLR4/p65 pathway deregulates β-catenin abundance in intestinal epithelial cells (IECs) from human NEC patients. The cell adhesion molecule β-catenin plays a crucial role in transcriptional activation of proliferation and cell growth in intestinal epithelial cells (IECs). It has been shown that β-catenin acts either as a pro-or anti-inflammatory mediator in a cell and tissue specific behavior. This study aims to elucidate the effects of stabilized β-catenin upon lipopolysaccharide (LPS) induced inflammatory signaling in IECs.

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摘要 DGKCH

患有坏死性小肠结肠炎（NEC）的人类早产儿肠道内毒素耐受性受损，但其根本机制仍不清楚。TLR4/p65通路的激活会降低人类NEC患者肠上皮细胞（IECs）中β-catenin的丰度。细胞粘附分子β-catenin在肠上皮细胞（IECs）增殖和细胞生长的转录激活过程中起着至关重要的作用。研究表明，β-catenin 可作为一种促炎或抗炎介质，具有细胞和组织特异性。本研究旨在阐明稳定的β-catenin对IECs中脂多糖（LPS）诱导的炎症信号转导的影响。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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