Gut microbiome–mediated bile acid metabolism regulates liver cancer via NKT cells
Chi Ma(National Institutes of Health), Miaojun Han(National Institutes of Health), Bernd Heinrich(National Institutes of Health), Qiong Fu(National Institutes of Health), Qianfei Zhang(National Institutes of Health), Milan Sandhu(National Institutes of Health), David Agdashian(National Institutes of Health), Masaki Terabe(National Institutes of Health), Jay A. Berzofsky(National Institutes of Health), Valerie Fako(National Institutes of Health), Thomas Ritz(RWTH Aachen University), Thomas Longerich(Heidelberg University), Casey M. Theriot(North Carolina State University), John A. McCulloch(National Institutes of Health), Soumen Roy(National Institutes of Health), Wuxing Yuan(National Institutes of Health), Vishal Thovarai(National Institutes of Health), Shurjo K. Sen(National Institutes of Health), Mathuros Ruchirawat(Chulabhorn Research Institute), Firouzeh Korangy(National Institutes of Health), Xin Wei Wang(National Institutes of Health), Giorgio Trinchieri(National Institutes of Health), Tim F. Greten(National Institutes of Health)
Cited by 1,467
Abstract
Bile acids and liver cancer Liver cancer is a leading cause of cancer-related deaths in the United States. The composition of the gut microbiome influences many human diseases, including liver inflammatory disorders. Ma et al. found that commensal gut bacteria can recruit the immune system to control the growth of liver tumors in mice (see the Perspective by Hartmann and Kronenberg). Clostridium species modified bile acids to signal liver sinusoidal endothelial cells to produce the chemokine CXCL16. This recruited natural killer T (NKT) immune cells to perform antitumor surveillance of the liver. Growth of both primary and metastatic cancer was reduced by NKT cell–driven killing. Science , this issue p. eaan5931 ; see also p. 858