@article{194a12cf182b4e3a9df28173dd0704b4,
title = "Intestinal Dysbiosis and Biotin Deprivation Induce Alopecia through Overgrowth of Lactobacillus murinus in Mice",
abstract = "Metabolism by the gut microbiota affects host physiology beyond the gastrointestinal tract. Here, we find that antibiotic-induced dysbiosis, in particular, overgrowth of Lactobacillus murinus (L. murinus), impaired gut metabolic function and led to the development of alopecia. While deprivation of dietary biotin per se did not affect skin physiology, its simultaneous treatment with vancomycin resulted in hair loss in specific pathogen-free (SPF) mice. Vancomycin treatment induced the accumulation of L. murinus in the gut, which consumes residual biotin and depletes available biotin in the gut. Consistently, L. murinus induced alopecia when monocolonized in germ-free mice fed a biotin-deficient diet. Supplementation of biotin can reverse established alopecia symptoms in the SPF condition, indicating that L. murinus plays a central role in the induction of hair loss via a biotin-dependent manner. Collectively, our results indicate that luminal metabolic alterations associated with gut dysbiosis and dietary modifications can compromise skin physiology.",
keywords = "Lactobacillus murinus, alopecia, biotin-deficiency, dysbiosis, gut microbiota, metabolome, microbiome",
author = "Atsushi Hayashi and Yohei Mikami and Kentaro Miyamoto and Nobuhiko Kamada and Toshiro Sato and Shinta Mizuno and Makoto Naganuma and Toshiaki Teratani and Ryo Aoki and Shinji Fukuda and Wataru Suda and Masahira Hattori and Masayuki Amagai and Manabu Ohyama and Takanori Kanai",
note = "Funding Information: We thank Drs. Hiroki Kiyohara, Mari Arai, Makoto Mutaguchi, Keiko Ono, Takeru Amiya, Takahiro Suzuki, Moeko Nakashima (Keio University), Tetsuro Kobayashi, and Keisuke Nagao (NIH) for technical assistance. This study was supported in part by grants-in-aid for Scientific Research (15H02534), Scientific Research on Priority Areas, Exploratory Research, and Creative Scientific Research from the Japanese Ministry of Education, Culture, Sports, Science and Technology ; the Japanese Ministry of Health, Labour and Welfare ; Japan Agency for Medical Research and Development (AMED) (AMED-CREST; 16gm1010003h0001 ); Miyarisan Pharmaceutical Co., Ltd ; Ezaki Glico Co., Ltd. ; and the Keio University Medical Fund . A.H. and K.M. are supported by Miyarisan Pharmaceutical Co., Ltd. Y.M. is supported by research fellowships of Japan Society for the Promotion of Science . R.A. is supported by Ezaki Glico Co., Ltd. Publisher Copyright: {\textcopyright} 2017",
year = "2017",
month = aug,
day = "15",
doi = "10.1016/j.celrep.2017.07.057",
language = "English",
volume = "20",
pages = "1513--1524",
journal = "Cell Reports",
issn = "2211-1247",
publisher = "Cell Press",
number = "7",
}