| Literature DB >> 33432149 |
Se-Hoon Lee1,2, Sung-Yup Cho3,4, Youngmin Yoon5, Changho Park6, Joon-Suk Park7, George M Weinstock8, Charles Lee8,9,10, Jinyoung Sohn6, Jin-Ju Jeong6, Bu-Nam Jeon6, Mongjoo Jang6, Choa An6, Suro Lee6, Yun Yeon Kim6, Gihyeon Kim5, Sujeong Kim5, Yunjae Kim5, Gwang Bin Lee11, Eun Ju Lee6, Sang Gyun Kim6, Hong Sook Kim1, Yeongmin Kim5, Hyun Kim5, Hyun-Suk Yang12, Sarang Kim12, Seonggon Kim7, Hayung Chung13, Myeong Hee Moon11, Myung Hee Nam13, Jee Young Kwon8, Sungho Won14, Kyoung Wan Yoon15,16, Hansoo Park17,18.
Abstract
The gut microbiome can influence the development of tumours and the efficacy of cancer therapeutics1-5; however, the multi-omics characteristics of antitumour bacterial strains have not been fully elucidated. In this study, we integrated metagenomics, genomics and transcriptomics of bacteria, and analyses of mouse intestinal transcriptome and serum metabolome data to reveal an additional mechanism by which bacteria determine the efficacy of cancer therapeutics. In gut microbiome analyses of 96 samples from patients with non-small-cell lung cancer, Bifidobacterium bifidum was abundant in patients responsive to therapy. However, when we treated syngeneic mouse tumours with commercial strains of B. bifidum to establish relevance for potential therapeutic uses, only specific B. bifidum strains reduced tumour burden synergistically with PD-1 blockade or oxaliplatin treatment by eliciting an antitumour host immune response. In mice, these strains induced tuning of the immunological background by potentiating the production of interferon-γ, probably through the enhanced biosynthesis of immune-stimulating molecules and metabolites.Entities:
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Year: 2021 PMID： 33432149 DOI： 10.1038/s41564-020-00831-6
Source DB: PubMed Journal: Nat Microbiol ISSN： 2058-5276 Impact factor: 17.745