Our gastrointestinal (GI) tract represents perhaps the most “contaminated” environment our bodies could encounter, being home to ~ 10 trillion microbes across thousands of species, collectively termed the “commensal microbiota.” Incredibly, despite their close association with our tissues, our bodies normally not only tolerate these microbes (mostly bacteria), but require them for proper development and function of the GI tract, and even beyond. However, in some cases, this mutualistic interaction fails, leading potentially to disease.
My research centers on the intestinal mucus system, a network of glycoproteins manufactured and secreted by a group of specialized intestinal cells, and how defects in this system contribute to susceptibility to infections, inflammatory bowel disease (IBD), and gastrointestinal tumors. To study this, we employ a repertoire of specialized skills to probe host-microbiota interactions in disease causation, including functional analysis of mucus glycoproteins, metagenomimcs, metatranscriptomics and state-of-the-art imaging and mouse genetic modeling. Our research has provided novel insights into how the intestinal mucin proteins with sugars (aka O-glycans) promote mucus barrier function that keeps the microbiota at a “healthy distance” from the gut, and prevent diseases such as IBD and colon cancer.
My current studies address how mucin-type O-glycans impact the structure and function of microbial communities in the gut, and how O-glycans regulate formation and function of the intestinal mucus system. The goals of this work aim to increase our knowledge of the fundamental roles of mucins and their O-glycans in the gut, and devise novel methods of intervention to boost their protective capacities in IBD and cancer patients.
B.Sc (Biology), University of Northern British Columbia, Prince George, BC, 2001
- Research Assistant with Dr. Chow H. Lee, Sept. 2001 – Aug. 2004
Ph.D. (Experimental Medicine), Univeristy of British Columbia, Vancouver, BC 2010
Joined OMRF Scientific Staff in 2011
Bergstrom K, Fu J, Johansson ME, Liu X, Gao N, Wu Q, Song J, McDaniel JM, McGee S, Chen W, Braun J, Hansson GC, Xia L. Core 1- and 3-derived O-glycans collectively maintain the colonic mucus barrier and protect against spontaneous colitis in mice. Mucosal Immunol. 2017 Jan;10(1):91-103. Epub 2016 May 4. (Includes cover figure for this issue.) PMCID: PMC5097036
Bergstrom K†, Perez-Munoz M†, Peng V, Schmaltz R, Jimenez-Cardona R, Marsteller N, McGee S, Clavel T, Ley R, Xia L*, Peterson D.* Discordance between changes in the gut microbiota and pathogenicity in a mouse model of spontaneous colitis. Gut Microbes. 2014 May-Jun;5(3):286-95. PMCID: PMC4153765
Bergstrom K†, Liu X†, Zhao Y†, Gao N, Wu Q, Song K, Cui Y, Li Y, McDaniel JM, McGee S, Chen W, Huycke MM, Houchen CW, Zenewicz LA, West CM, Chen H, Braun J, Fu J*, Xia L*. Defective Intestinal Mucin-Type O-Glycosylation Causes Spontaneous Colitis-Associated Cancer in Mice. 2016 Jul;151(1):152-64. PMCID: PMC5068133
Bergstrom K†, Gao N†, Fu J, Xie B, Chen W, Xia, L. Loss of intestinal O-glycans promotes spontaneous duodenal tumors. Am J Physiol Gastrointest Liver Physiol. 2016 Jul 1;311(1):G74-83. PMCID: PMC4967177
Song K, Fu J, Song J, Herzog BH, Bergstrom K, Kondo Y, McDaniel JM, McGee S, Silasi-Mansat R, Lupu F, Chen H, Bagavant H, Xia L. Loss of mucin-type O-glycans impairs the integrity of the glomerular filtration barrier in the mouse kidney. J Biol Chem. 2017 Oct 6;292(40):16491-7. PMCID: PMC5633109
Bergstrom K, Kissoon-Singh V, Gibson DL, Ma C, Montero M, Sham HP, Ryz N, Huang JT, Velcich A, Finlay BB, Chadee K, Vallance BA. Muc2 protects against lethal infectious colitis by disassociating pathogenic and commensal bacteria from the colonic mucosa. PLoS Pathog. 2010 May;6(5): e1000902. PMCID: PMC2869315
† = equal contributions; * = co-senior author
Cardiovascular Biology Research Program
Oklahoma Medical Research Foundation
825 N.E. 13th Street, MS 45
Oklahoma City, OK 73104-5005
Phone: (405) 271-3979
Fax: (405) 271-3137