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P1-195 Roles of NAG-1 in Epithelial Toxicity of Foodborne Carrageenan as IBD-Like Symptom Trigger

Sunday, July 26, 2015
Exhibit Hall (Oregon Convention Center)
Juil KIM
Hye Jin CHOI , Dept of Biomedical Sciences, Pusan National University , Yangsan , Korea, Republic of (South)
Yuseok Moon , Dept. of Biomedical Sciences, Pusan National University , Yangsan , Korea, Republic of (South)
Introduction: Carrageenan (CGN), a widely used food additive, has been shown to injure the epithelial barrier in animal models. This type of damage is a clinical feature of inflammatory bowel disease (IBD) in humans. 

Purpose: In the present study, the effects of CGN on pro-apoptotic responses associated with NSAID-activated gene 1 (NAG-1) regulation in human enterocytes were evaluated. 

Methods: Human and murine entrocytes were assessed using different tools of cell biology and immunology.

Results: CGN up-regulated the expression of NAG-1 that promoted epithelial cell apoptosis. Although NAG-1 induction was dependent on pro-apoptotic p53 protein, the pro-survival protein ATF3 was negatively regulated by p53 expression. However, NAG-1 enhanced the expression of the pro-survival protein ATF3 in enterocytes exposed to CGN. Functionally, NAG-1-mediated epithelial cell apoptosis was counteracted by the pro-survival action of ATF3 in response to CGN exposure. 

Significance: These findings demonstrated that the counterbalance between NAG-1 and ATF3 is critical for deciding the fate of enterocytes under the food chemical stress (This study was supported by a grant of the Korean Health Technology R&D Project, Ministry of Health &Welfare, Republic of Korea (HI13C0259).

Back to: Poster Session 1 – Laboratory and Detection Methods, Low-water Activity; Retail and Food Service Safety; Seafood; Communication Outreach and Education; Produce; Food Toxicology; Non-microbial Food Safety; Food Defense; Microbial Food Spoilage
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