Glucose promotes regulatory T cell differentiation to maintain intestinal homeostasis
Yu Yu,
Wenjing Yang,
Tianming Yu,
Xiaojing Zhao,
Zheng Zhou,
Yanbo Yu,
Lifeng Xiong,
Hui Yang,
Anthony J. Bilotta,
Suxia Yao,
George Golovko,
Agustin Plasencia,
Francisco J. Quintana,
Liang Zhou,
Yanqing Li,
Yingzi Cong
Affiliations
Yu Yu
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA; Department of Gastroenterology, Qilu Hospital, Shandong University, Jinan 250012, P.R. China
Wenjing Yang
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Tianming Yu
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Xiaojing Zhao
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Zheng Zhou
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Yanbo Yu
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA; Department of Gastroenterology, Qilu Hospital, Shandong University, Jinan 250012, P.R. China
Lifeng Xiong
Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA
Hui Yang
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Anthony J. Bilotta
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
Suxia Yao
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA
George Golovko
Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA
Agustin Plasencia
Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard University Medical School, Boston, MA 02115, USA
Francisco J. Quintana
Ann Romney Center for Neurologic Diseases, Brigham and Women’s Hospital, Harvard University Medical School, Boston, MA 02115, USA
Liang Zhou
Department of Infectious Diseases and Immunology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA
Yanqing Li
Department of Gastroenterology, Qilu Hospital, Shandong University, Jinan 250012, P.R. China
Yingzi Cong
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston, TX 77555, USA; Corresponding author
Summary: Glucose, the critical energy source in the human body, is considered a potential risk factor in various autoimmune diseases when consumed in high amounts. However, the roles of glucose at moderate doses in the regulation of autoimmune inflammatory diseases and CD4+ T cell responses are controversial. Here, we show that while glucose at a high concentration (20% w/v) promotes intestinal inflammation, it suppresses colitis at a moderate dose (6% w/v), which increases the proportion of intestinal regulatory T (Treg) cells but does not affect effector CD4+ T cells. Glucose treatment promotes Treg cell differentiation but it does not affect Treg stability. Feeding glucose alters gut microbiota compositions, which are not involved in the glucose induction of Treg cells. Glucose promotes aryl hydrocarbon receptor (AhR) activation to induce Treg polarization. These findings reveal the different effects of glucose at different doses on the intestinal immune response.
