Oxidized polyunsaturated fatty acid promotes colitis and colitis-associated tumorigenesis in mice

结肠炎 偶氮甲烷 多不饱和脂肪酸 炎症性肠病 癌变 结直肠癌 医学 TLR4型 基因剔除小鼠 免疫学 癌症研究 内科学 受体 炎症 脂肪酸 生物 癌症 生物化学 疾病
作者
Weicang Wang,Yuxin Wang,Katherine Z. Sanidad,Yige Wang,Jianan Zhang,Wenqi Yang,Quancai Sun,Ipek Bayram,Renhua Song,Haixia Yang,David Johnson,Heather L. Sherman,Daeyoung Kim,Lisa M. Minter,Justin Wong,Melody Y. Zeng,Eric A. Decker,Guodong Zhang
出处
期刊:Journal of Crohn's and Colitis [Oxford University Press]
标识
DOI:10.1093/ecco-jcc/jjae148
摘要

Abstract Background and Aims Human studies suggest that a high intake of polyunsaturated fatty acid (PUFA) is associated with an increased risk of inflammatory bowel disease (IBD). PUFA is highly prone to oxidation. To date, it is unclear whether unoxidized or oxidized PUFA is involved in the development of IBD. Here, we aim to compare the effects of unoxidized PUFA vs. oxidized PUFA on the development of IBD and associated colorectal cancer. Methods We evaluated the effects of unoxidized and oxidized PUFA on dextran sodium sulfate (DSS)- and IL-10 knockout-induced colitis, and azoxymethane (AOM)/DSS-induced colon tumorigenesis in mice. Additionally, we studied the roles of gut microbiota and Toll-like receptor 4 (TLR4) signaling involved. Results Administration of a diet containing oxidized PUFA, at human consumption-relevant levels, increases the severity of colitis and exacerbates the development of colitis-associated colon tumorigenesis in mice. Conversely, a diet rich in unoxidized PUFA doesn’t promote colitis. Furthermore, oxidized PUFA worsens colitis-associated intestinal barrier dysfunction and leads to increased bacterial translocation, and it fails to promote colitis in Toll-like receptor 4 (TLR4) knockout mice. Finally, oxidized PUFA alters the diversity and composition of gut microbiota, and it fails to promote colitis in mice lacking the microbiota. Conclusions These results support that oxidized PUFA promotes the development of colitis and associated tumorigenesis in mouse models via TLR4- and gut microbiota-dependent mechanisms. Our findings highlight the potential need to update regulation policies and industrial standards for oxidized PUFA levels in food.
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