Eugene B. Chang, M.D.


  • Martin Boyer Professor, Department of Medicine, Department of Cell Physiology, Cancer Research Center, Committee on Immunology, Committe on Molecular Metabolism and Nutrition, Committee on Clinical and Translational Science
  • Associate Section Chief for Research


M.D., The University of Chicago
B.A., Johns Hopkins University


The University of Chicago
KCBD 9130
900 East 57th Street 
Chicago, Illinois 60637

Phone:  (773) 702-6458

Website (UC Hospitals)


Intestinal Adaptation Mechanism for Nutrient and Electrolyte Absorption in Disease and Hormonal Regulation of Intestinal Absorption and Secretion

We have two major research interests:

1. The focus of our group is on the study of the intestinal microbes, particularly how they interact with the host. This relationship is fundamental to our health and, when perturbed, the consequences can be catastrophic.  In this regard, the emergence of “new age” disorders like diabetes, obesity, metabolic syndrome, cancer and autoimmune disorders over the past century may be related to large shifts in the composite human microbiome caused by changes in the environment and life styles. In genetically susceptible individuals, these factors can potentially trigger events that disturb immune and metabolic homeostasis, initiating the development of disease. Our efforts are therefore directed towards gaining a better understanding of what factors are involved in the selection and assembly of intestinal microbes, and how they can be used to reshape the enteric microbiome to prevent and treat disease. We employ cutting edge approaches that include cultivation-dependent and –independent technologies for microbial analysis, genetically modified and gnotobiotic mouse models, metabolic and functional measurements, and advanced bioinformatic tools to investigate both host and microbiome.

2. The role of heat shock protein in maintaining intestinal and immune homeostasis Heat shock proteins (HSPs) are a highly conserved family of multifunctional molecules. They play a role in mucosal cytoprotection, host-microbe interactions, innate immunity, cancer initiation and development, and in autophagy. Although many types are constitutively expressed, some, such as HSP70 and HSP25, are rapidly induced and preferentially synthesized under conditions of cellular stress and injury. Their physiological expression in the gut is maintained by cues and signals provided by the enteric microbiota.  In epithelial cells, their induction protects against toxic, oxidant, and thermal injury. Our laboratory, therefore, is investigating cellular and molecular mechanisms that mediate their cytoprotective effects in the context of mucosal inflammation. These studies involve correlations of molecular and biochemical techniques with physiological findings and imaging analysis.


Bellaguarda, E. and E. B. Chang (2015). "IBD and the gut microbiota--from bench to personalized medicine." Curr Gastroenterol Rep 17(4): 15.

Huang, E. Y., T. Inoue, V. A. Leone, S. Dalal, K. Touw, Y. Wang, M. W. Musch, B. Theriault, K. Higuchi, S. Donovan, J. Gilbert and E. B. Chang (2015). "Using corticosteroids to reshape the gut microbiome: implications for inflammatory bowel diseases." Inflamm Bowel Dis 21(5): 963-972.

Leone, V., S. M. Gibbons, K. Martinez, A. L. Hutchison, E. Y. Huang, C. M. Cham, J. F. Pierre, A. F. Heneghan, A. Nadimpalli, N. Hubert, E. Zale, Y. Wang, Y. Huang, B. Theriault, A. R. Dinner, M. W. Musch, K. A. Kudsk, B. J. Prendergast, J. A. Gilbert and E. B. Chang (2015). "Effects of diurnal variation of gut microbes and high-fat feeding on host circadian clock function and metabolism." Cell Host Microbe 17(5): 681-689.

Lu, L., Y. Yu, Y. Guo, Y. Wang, E. B. Chang and E. C. Claud (2015). "Transcriptional modulation of intestinal innate defense/inflammation genes by preterm infant microbiota in a humanized gnotobiotic mouse model." PLoS One 10(4): e0124504.

Wu, S., Y. G. Zhang, R. Lu, Y. Xia, D. Zhou, E. O. Petrof, E. C. Claud, D. Chen, E. B. Chang, G. Carmeliet and J. Sun (2015). "Intestinal epithelial vitamin D receptor deletion leads to defective autophagy in colitis." Gut 64(7): 1082-1094.