期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 114, 期 38, 页码 10178-10183出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1712837114
关键词
surfactant protein D; gut microbiota; gallbladder; colitis; glucocorticoids
资金
- Ministry of Education, Culture, Sports, Science [15638461]
- Japan Agency for Medical Research and Development [15656877]
- Nakajima Foundation
- Uehara Memorial Foundation
- BONAC Corporation
- Kyowa Hakko Kirin Co.
- Grants-in-Aid for Scientific Research [16K09537, 15H05787] Funding Source: KAKEN
The commensal microbiota within the gastrointestinal tract is essential in maintaining homeostasis. Indeed, dysregulation in the repertoire of microbiota can result in the development of intestinal immune-inflammatory diseases. Further, this immune regulation by gut microbiota is important systemically, impacting health and disease of organ systems beyond the local environment of the gut. What has not been explored is how distant organs might in turn shape the microbiota via microbe-targeted molecules. Here, we provide evidence that surfactant protein D (SP-D) synthesized in the gallbladder and delivered into intestinal lumen binds selectively to species of gut commensal bacteria. SP-D-deficient mice manifest intestinal dysbiosis and show a susceptibility to dextran sulfate sodium-induced colitis. Further, fecal transfer from SP-D-deficient mice to wild-type, germ-free mice conveyed colitis susceptibility. Interestingly, colitis caused a notable increase in Sftpd gene expression in the gallbladder, but not in the lung, via the activity of glucocorticoids produced in the liver. These findings describe a unique mechanism of interorgan regulation of intestinal immune homeostasis by SP-D with potential clinical implications such as cholecystectomy.
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