Lactose drives Enterococcus expansion to promote graft-versus-host disease.
Christoph K Stein-ThoeringerKatherine NicholsA LazrakMelissa DocampoA E SlingerlandJ B SlingerlandA G ClurmanG ArmijoAntonio L C GomesYusuke ShonoAnna StaffasMarina Burgos da SilvaS M DevlinKate A MarkeyD BajicR PinedoA TsakmaklisEric R LittmannAlessandro PastoreYing TaurSebastien MonetteM E ArcilaA J PickardM MaloyRoberta J WrightLuigi A AmorettiE FontanaDung PhamM A JamalD WeberA D SungDaigo HashimotoC ScheidJoao B XavierJulia A MessinaK RomeroM LewAmy T BushLauren M BohannonK HayasakaYuta HasegawaM J G T VehreschildJ R CrossD M PonceMiguel-Ángel PeralesSergio A GiraltRobert R JenqTakanori TeshimaE HollerNelson J ChaoEric G PamerJonathan U PeledMarcel R M van den BrinkPublished in: Science (New York, N.Y.) (2020)
Disruption of intestinal microbial communities appears to underlie many human illnesses, but the mechanisms that promote this dysbiosis and its adverse consequences are poorly understood. In patients who received allogeneic hematopoietic cell transplantation (allo-HCT), we describe a high incidence of enterococcal expansion, which was associated with graft-versus-host disease (GVHD) and mortality. We found that Enterococcus also expands in the mouse gastrointestinal tract after allo-HCT and exacerbates disease severity in gnotobiotic models. Enterococcus growth is dependent on the disaccharide lactose, and dietary lactose depletion attenuates Enterococcus outgrowth and reduces the severity of GVHD in mice. Allo-HCT patients carrying lactose-nonabsorber genotypes showed compromised clearance of postantibiotic Enterococcus domination. We report lactose as a common nutrient that drives expansion of a commensal bacterium that exacerbates an intestinal and systemic inflammatory disease.
Keyphrases
- biofilm formation
- end stage renal disease
- endothelial cells
- risk factors
- ejection fraction
- stem cell transplantation
- cell cycle arrest
- chronic kidney disease
- pseudomonas aeruginosa
- bone marrow
- prognostic factors
- candida albicans
- cardiovascular events
- peritoneal dialysis
- cardiovascular disease
- low dose
- skeletal muscle
- cell death
- cell proliferation
- cystic fibrosis
- high dose
- patient reported outcomes
- pluripotent stem cells