オカザキ　ケン   Okazaki Ken   岡崎　賢    所属   医学部 医学科（東京女子医科大学病院）    職種   教授・基幹分野長
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Alcohol consumption induces murine osteoporosis by downregulation of natural killer T-like cell activity.
掲載誌名	正式名：Immunity, inflammation and disease 略　 称：Immun Inflamm Dis ISSNコード：20504527/20504527
掲載区分	国外
巻・号・頁	9(4),pp.1370-1382
著者・共著者	NRUO Munehiko, NEGISHI Yasuyuki, OKUDA Takahisa, KATSUYAMA Midori, OKAZAKI Ken, MORITA Rimpei
発行年月	2021/12
概要	INTRODUCTION:Chronic alcohol consumption (CAC) can induce several deleterious effects on the body, including the promotion of osteoporosis; however, the immunological mechanism underlying alcohol-induced osteoporosis is still unclear.METHODS:We administered alcohol to mice for 4 weeks as the experimental CAC model and analyzed the bone and immune cells that are located in the vicinity of a bone.RESULTS:IL-4 is known to be a suppressive factor for osteoclastogenesis, and we found that natural killer T (NKT)-like cells, which showed NK1.1-positive, CD3-positive, and α-galactosylceramide-loaded CD1d tetramer-negative, produced IL-4 more effectively than CD4+ T and natural killer (NK) cells. The alcohol consumption facilitated a significant decrease of bone mineral density with the upregulation of nuclear factor of activated T cells 1 and receptor activator of NF-κB ligand expression. Meanwhile, we confirmed that alcohol consumption suppressed the activity of antigen-presenting cells (APCs) and NKT-like cells, leading to decreased IL-4 secretion. Moreover, these harmful effects of alcohol consumption were reduced by simultaneous treatment with a glycolipid antigen OCH.CONCLUSIONS:Our results indicate that the inactivation of innate immune cells, APCs, and NKT-like cells are likely to be crucial for alcohol-induced osteoporosis and provide a new therapeutic approach for preventing osteoporosis.
DOI	10.1002/iid3.485
PMID	34214248