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毒素诱导小鼠肠上皮细胞系中E-钙黏蛋白的顺序性蛋白水解及炎症反应。

Toxin Induces Sequential Proteolysis of E-Cadherin and Inflammatory Response in Mouse Intestinal Epithelial Cell Line.

作者信息

Kim Woo-Seung, Hwang Soonjae, Gwon Sun-Yeong, Jo Minjeong, Yoo Sang-Hyeon, Hong Jiyun, Jang Ha-Neul, Hong Ju-Eun, Kang Da-Hye, Yun Miyong, Rhee Ki-Jong

机构信息

Department of Biomedical Laboratory Science, College of Software Digital Healthcare Convergence, Yonsei University at MIRAE Campus, Wonju 26493, Republic of Korea.

Department of Biochemistry, Lee Gil Ya Cancer and Diabetes Institute, College of Medicine, Gachon University, 155 Gaetbeol-ro, Inchon 21999, Republic of Korea.

出版信息

Microorganisms. 2025 Mar 28;13(4):781. doi: 10.3390/microorganisms13040781.

DOI:10.3390/microorganisms13040781
PMID:40284619
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12029241/
Abstract

Enterotoxigenic (ETBF) is an intestinal bacterium that secretes the metalloprotease toxin (BFT), which induces E-cadherin cleavage and interleukin-8 secretion in human intestinal epithelial cell lines. ETBF-induced E-cadherin cleavage is proposed to be the underlying reason for the promotion of colitis in ETBF-infected mice. However, a BFT-responsive murine cell line has not yet been reported. In the current study, we report that the mouse colonic epithelial cell line CMT93 undergoes E-cadherin ectodomain cleavage, cell rounding, and proliferation in response to BFT treatment. The amino acid sequence of the putative cleavage site of E-cadherin is identical in both BFT-responsive (CMT93) and BFT-nonresponsive (MSIE, CT26, YAMC, and B16) cell lines, suggesting that the E-cadherin amino acid sequence is not responsible for this observation. After E-cadherin ectodomain cleavage, the membrane-bound intracellular E-cadherin domain underwent cleavage by γ-secretase and was subsequently degraded by the proteasome. Moreover, BFT induced the secretion of two chemokines (LIX and KC) and the formation of soluble TNFR1 in the CMT93 cell line. The identification of a BFT-responsive murine cell line may be used to elucidate the mechanism of ETBF pathogenesis in ETBF murine infection models.

摘要

产肠毒素脆弱拟杆菌（ETBF）是一种肠道细菌，可分泌金属蛋白酶毒素（BFT），该毒素可诱导人肠道上皮细胞系中的E-钙黏蛋白裂解和白细胞介素-8分泌。ETBF诱导的E-钙黏蛋白裂解被认为是ETBF感染小鼠中结肠炎进展的潜在原因。然而，尚未报道对BFT有反应的小鼠细胞系。在本研究中，我们报告小鼠结肠上皮细胞系CMT93在接受BFT处理后会发生E-钙黏蛋白胞外域裂解、细胞变圆和增殖。E-钙黏蛋白假定裂解位点的氨基酸序列在对BFT有反应的（CMT93）和对BFT无反应的（MSIE、CT26、YAMC和B16）细胞系中是相同的，这表明E-钙黏蛋白氨基酸序列与这一现象无关。E-钙黏蛋白胞外域裂解后，膜结合的细胞内E-钙黏蛋白结构域被γ-分泌酶裂解，随后被蛋白酶体降解。此外，BFT在CMT93细胞系中诱导了两种趋化因子（LIX和KC）的分泌以及可溶性TNFR1的形成。对BFT有反应的小鼠细胞系的鉴定可用于阐明ETBF小鼠感染模型中ETBF发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/73f2fa4346bb/microorganisms-13-00781-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/bfe66cb4bf14/microorganisms-13-00781-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/0f68074df260/microorganisms-13-00781-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/57c08151f812/microorganisms-13-00781-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/ad943ea0a7ee/microorganisms-13-00781-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/73f2fa4346bb/microorganisms-13-00781-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/bfe66cb4bf14/microorganisms-13-00781-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/0f68074df260/microorganisms-13-00781-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/57c08151f812/microorganisms-13-00781-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/ad943ea0a7ee/microorganisms-13-00781-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/750b/12029241/73f2fa4346bb/microorganisms-13-00781-g006.jpg

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Toxin Induces Intestinal Epithelial Cell Secretion of Interleukin-8 by the E-Cadherin/β-Catenin/NF-κB Dependent Pathway.毒素通过E-钙黏蛋白/β-连环蛋白/NF-κB依赖途径诱导肠上皮细胞分泌白细胞介素-8。
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The Autophagic Route of E-Cadherin and Cell Adhesion Molecules in Cancer Progression.E-钙黏蛋白和细胞黏附分子在癌症进展中的自噬途径
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