Pro-inflammatory NF-κB and early growth response gene 1 regulate epithelial barrier disruption by food additive carrageenan in human intestinal epithelial cells

Toxicology Letters
Hye Jin ChoiYuseok Moon

Abstract

The widely used food additive carrageenan (CGN) has been shown to induce intestinal inflammation, ulcerative colitis-like symptoms, or neoplasm in the gut epithelia in animal models, which are also clinical features of human inflammatory bowel disease. In this study, the effects of CGN on pro-inflammatory transcription factors NF-κB and early growth response gene 1 product (EGR-1) were evaluated in terms of human intestinal epithelial barrier integrity. Both pro-inflammatory transcription factors were elevated by CGN and only NF-κB activation was shown to be involved in the induction of pro-inflammatory cytokine interleukin-8. Moreover, the integrity of the in vitro epithelial monolayer under the CGN insult was maintained by both activated pro-inflammatory transcription factors NF-κB and EGR-1. Suppression of NF-κB or EGR-1 aggravated barrier disruption by CGN, which was associated with the reduced gene expression of tight junction component zonula occludens 1 and its irregular localization in the epithelial monolayer.

References

Jul 1, 1992·Scandinavian Journal of Gastroenterology·H S Kim, A Berstad
Jan 1, 1987·Critical Reviews in Toxicology·T IshiokaK Wakabayashi
Jan 31, 1998·The Journal of Biological Chemistry·M M AhmedV M Rangnekar
Jul 8, 1998·Proceedings of the National Academy of Sciences of the United States of America·S F YanD Stern
Feb 15, 2000·The Journal of Biological Chemistry·N R Chapman, N D Perkins
May 12, 2000·Alimentary Pharmacology & Therapeutics·S SzaboM Yoshida
Oct 25, 2001·Environmental Health Perspectives·J K Tobacman
Jun 27, 2003·American Journal of Physiology. Cell Physiology·Laurence J EganMartin F Kagnoff
Feb 26, 2004·Proceedings of the National Academy of Sciences of the United States of America·Laurence J EganMartin F Kagnoff
Feb 18, 2006·American Journal of Physiology. Gastrointestinal and Liver Physiology·Tetyana KhomenkoLongchuan Chen
Jun 15, 2006·Neuropathology : Official Journal of the Japanese Society of Neuropathology·Ying LiuZhu-Rong Ye
Nov 25, 2006·The Journal of Clinical Investigation·Alexander VisekrunaUlrich Steinhoff
Sep 1, 2007·Inflammatory Bowel Diseases·Thomas Karrasch, Christian Jobin
Oct 16, 2007·Applied and Environmental Microbiology·Laura Y Sifuentes, George D Di Giovanni
May 24, 2008·The Journal of Infectious Diseases·Cirle Alcantara WarrenRichard L Guerrant
Jun 17, 2009·Current Opinion in Gastroenterology·Martina E Spehlmann, Lars Eckmann
Jun 23, 2009·Annals of the New York Academy of Sciences·Joerg D SchulzkeMichael Fromm
Jul 28, 2009·Current Opinion in Pharmacology·Karen L Edelblum, Jerrold R Turner
Jul 21, 2011·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·Fanxia ShenHua Su

❮ Previous
Next ❯

Citations

May 7, 2016·American Journal of Physiology. Gastrointestinal and Liver Physiology·Yuka MiyoshiTakuya Suzuki
Sep 8, 2020·Cell Communication and Signaling : CCS·Alexandre H LopesThiago M Cunha
May 17, 2017·Frontiers in Pediatrics·John Vincent MartinoLeah E Cahill
Apr 12, 2019·International Journal of Molecular Sciences·Kaiwen MuDavid D Kitts
Mar 25, 2020·Nutrients·Gina L TrakmanMichael A Kamm
Apr 26, 2018·EFSA Journal·UNKNOWN EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS)Birgit Dusemund
Jun 20, 2021·Comprehensive Reviews in Food Science and Food Safety·Fang LiuRobert W Li

❮ Previous
Next ❯

Related Concepts

Related Feeds

Anemia

Anemia develops when your blood lacks enough healthy red blood cells. Anemia of inflammation (AI, also called anemia of chronic disease) is a common, typically normocytic, normochromic anemia that is caused by an underlying inflammatory disease. Here is the latest research on anemia.

Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis