• Science · Nov 2019

    Lactose drives Enterococcus expansion to promote graft-versus-host disease.

    • C K Stein-Thoeringer, K B Nichols, A Lazrak, M D Docampo, A E Slingerland, J B Slingerland, A G Clurman, G Armijo, A L C Gomes, Y Shono, A Staffas, M Burgos da Silva, S M Devlin, K A Markey, D Bajic, R Pinedo, A Tsakmaklis, E R Littmann, A Pastore, Y Taur, S Monette, M E Arcila, A J Pickard, M Maloy, R J Wright, L A Amoretti, E Fontana, D Pham, M A Jamal, D Weber, A D Sung, D Hashimoto, C Scheid, J B Xavier, J A Messina, K Romero, M Lew, A Bush, L Bohannon, K Hayasaka, Y Hasegawa, VehreschildM J G TMJGTDepartment I of Internal Medicine, Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, University of Cologne, Cologne, Germany.German Center for Infection Research, Partner site Bonn-Cologne, Cologne, Germany.Department o, J R Cross, D M Ponce, M A Perales, S A Giralt, R R Jenq, T Teshima, E Holler, N J Chao, E G Pamer, J U Peled, and M R M van den Brink.
    • Department of Immunology, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
    • Science. 2019 Nov 29; 366 (6469): 1143-1149.

    AbstractDisruption 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.Copyright © 2019 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.

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