Triclocarban Exposure Exaggerates Spontaneous Colonic Inflammation in Il-10−/− Mice

Author:

Xie Minhao12,Zhang Hongna3,Wang Weicang2,Sherman Heather L4,Minter Lisa M45,Cai Zongwei3,Zhang Guodong25

Affiliation:

1. Collaborative Innovation Center for Modern Grain Circulation and Safety, College of Food Science and Engineering, Nanjing University of Finance and Economics, Nanjing 210023, China

2. Department of Food Science, University of Massachusetts, Amherst 01003, Massachusetts

3. State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong 999077, China

4. Department of Veterinary and Animal Sciences

5. Molecular and Cellular Biology Graduate Program, University of Massachusetts, Amherst 01003, Massachusetts

Abstract

Abstract Triclocarban (3,4,4′-trichlorocarbanilide, TCC) is a high-volume chemical used as an antimicrobial ingredient in many consumer and personal care products. In 2016, the Food and Drug Administration removed TCC from over-the-counter hand washing products. However, TCC remains approved to use in many other products and is a ubiquitous contaminant in the environment; furthermore, many common food crops can efficiently accumulate environmental TCC, resulting in potential human exposure through oral ingestion of contaminated food products. Therefore, human exposure to TCC could be a long-lasting and serious problem. A better understanding of its impact on human health could lead to important impact for public health and regulatory policy. Using a spontaneous colonic inflammation model in Il-10−/− mice, here we demonstrate that exposure to TCC, at doses relevant to human exposure, exaggerates spontaneous colonic inflammation in Il-10−/− mice, with reduced colon length, increase fecal concentration of lipocalin 2, enhanced gene expression of Il-6 and Ifn-γ in the colon, and exaggerated crypt damage in the colon. Collectively, these results support that TCC could be a potential environmental risk factor of colitis and associated gut diseases.

Funder

University of Massachusetts

General Research Fund

Hong Kong Research Grants Council

Publisher

Oxford University Press (OUP)

Subject

Toxicology

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