期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 209, 期 5, 页码 902-910出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20112408
关键词
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资金
- National Institutes of Health [R01-HL069929, R01-CA107096, R01-AI080455, RO1-AI042135, R37-AI039031, PO1-CA023766, R01-AI34495, R01-HL56067]
- United States Department of Defense USAMRAA [W81XWH-09-1-0294]
- Radiation Effects Research Foundation (RERF-NIAID)
- Experimental Therapeutics Center of Memorial Sloan-Kettering Cancer Center
- Lymphoma Foundation
- Alex's Lemonade Stand
- Geoffrey Beene Cancer Research Center at Memorial Sloan-Kettering Cancer Center
- Peter Solomon Fund
- Lucille Castori Center for Microbes, Inflammation, and Cancer
- Leonard Tow Foundation
Despite a growing understanding of the link between intestinal inflammation and resident gut microbes, longitudinal studies of human flora before initial onset of intestinal inflammation have not been reported. Here, we demonstrate in murine and human recipients of allogeneic bone marrow transplantation (BMT) that intestinal inflammation secondary to graft-versus-host disease (GVHD) is associated with major shifts in the composition of the intestinal microbiota. The microbiota, in turn, can modulate the severity of intestinal inflammation. In mouse models of GVHD, we observed loss of overall diversity and expansion of Lactobacillales and loss of Clostridiales. Eliminating Lactobacillales from the flora of mice before BMT aggravated GVHD, whereas reintroducing the predominant species of Lactobacillus mediated significant protection against GVHD. We then characterized gut flora of patients during onset of intestinal inflammation caused by GVHD and found patterns mirroring those in mice. We also identified increased microbial chaos early after allogeneic BMT as a potential risk factor for subsequent GVHD. Together, these data demonstrate regulation of flora by intestinal inflammation and suggest that flora manipulation may reduce intestinal inflammation and improve outcomes for allogeneic BMT recipients.
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