Professor of Pediatrics and Biochemistry & Molecular Medicine
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D. Brent Polk, MD, is Professor of Pediatrics and Biochemistry & Molecular Medicine; he served as chair of the Department of Pediatrics and Physician-in-Chief, Vice President for Academic Affairs and Director of The Saban Research Institute at CHLA. He also served as chair of pediatrics and vice dean for Child Health at the Keck School of Medicine of the University of Southern California.

Dr. Polk previously served as chief of the D. Brent Polk Division of Pediatric Gastroenterology, Hepatology and Nutrition, director of the Digestive Disease Research Center and a tenured professor of Pediatrics and Cell and Developmental Biology at Vanderbilt University Medical Center. He received a bachelor's degree in biology and chemistry from Ouachita University in Arkadelphia, Ark., and his medical degree from the University of Arkansas for Medical Sciences.

Clinical Interests

Digestive and nutritional diseases, inflammatory bowel diseases, Crohn's disease and ulcerative colitis


Medical School: 

University of Arkansas for Medical Sciences


University of Arkansas for Medical Sciences and Arkansas Childrens Hospital: Pediatrics


University of Arkansas for Medical Sciences and Arkansas Childrens Hospital: Pediatrics


Stanford University School of Medicine; Pediatric Gastroenterology and Nutrition



Pediatric Gastroenterology; American Board of Pediatrics

Medical Memberships: 

Alpha Omega Alpha (AOA)
American Academy of Pediatrics (AAP)
American Association for the Advancement of Science (AAAS)
American Gastroenterological Association (AGA)
American Pediatric Society (APS)
American Physiological Society (APS)
American Society for Biochemistry and Molecular Biology (ASBMB)
American Society for Cell Biology (ASCB)
American Society for Parenteral and Enteral Nutrition (ASPEN)
Crohn's & Colitis Foundation
Association of American Physicians (AAP)
Council of Delegates, Intestinal Disorders Section of AGA
Federation of American Societies for Experimental Biology (FASEB)
Gastroenterology Research Group (GRG)
North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition (NASPGHAN)
Royal College of Physicians of Edinburgh (RCP-E)
Society for Pediatric Research (SPR)

Medical Awards: 

American Gastroenterological Association Fellow, 2008
University of Arkansas College of Medicine, Distinguished Alumni Award, 2009
Grant W. Liddle Award, 2009
Who's Who in North American Education, 2012-2017
Council of Deans Fellows, Association of American Medical Colleges, 2014-2015
Shwachman Award, NASPGHAN, 2015
Mike Miller Memorial Award for Volunteer Excellence, Crohn's & Colitis Foundation, 2016
University of Arkansas College of Medicine, Hall of Fame, 2016
American Association for the Advancement of Science Fellow Election, 2016
Association of American Physicians Election, 2017
Alpha Omega Alpha Election, 2017
Royal College of Physicians of Edinburgh Fellow, 2017


Tumor Necrosis Factor Receptor 2 Restricts the Pathogenicity of CD8(+) T Cells in Mice With Colitis.
Punit S, Dubé PE, Liu CY, Girish N, Washington MK, Polk DB. Gastroenterology. 2015 Oct;149(4):993-1005.e2. doi: 10.1053/j.gastro.2015.06.004. Epub 2015 Jun 11. PMID: 26072395

Optical reconstruction of murine colorectal mucosa at cellular resolution.
Liu CY, Dubé PE, Girish N, Reddy AT, Polk DB. Am J Physiol Gastrointest Liver Physiol. 2015 May 1;308(9):G721-35. doi: 10.1152/ajpgi.00310.2014. Epub 2015 Feb 26. PMID: 25721303

Redeeming an old foe: protective as well as pathophysiological roles for tumor necrosis factor in inflammatory bowel disease.
Dubé PE, Punit S, Polk DB. Am J Physiol Gastrointest Liver Physiol. 2015 Feb 1;308(3):G161-70. doi: 10.1152/ajpgi.00142.2014. Epub 2014 Dec 4. Review. PMID:25477373

Neonatal colonization of mice with LGG promotes intestinal development and decreases susceptibility to colitis in adulthood.
Yan F, Liu L, Cao H, Moore DJ, Washington MK, Wang B, Peek RM, Acra SA, and Polk DB. Mucosal Immunol. 2016 Apr 20. doi: 10.1038/mi.2016.43 PMID: 27095077

An LGG-derived protein promotes IgA production through upregulation of APRIL expression in intestinal epithelial cells.
Wang Y, Liu L, Moore, DJ, Shen, X, Peek, RM, Acra, SA, Li, H, Ren, X, Polk, DB, and Yan, F. Mucosal. Immunol. 2016 Jun 29. doi: 10.1038/mi.2016.57 PMID: 27353252

Research Interests: 

Intestinal Injury, Regenerative Medicine, Devlopmental Biology, Mucosal Immunology, Microbiome, Probiotics


Research Topics

  • Regulation of the growth and development of the intestine

  • Childhood inflammatory bowel disease

Research Overview

Our laboratory studies the regulation of the growth and development of the intestine as it relates to injury, inflammation, regeneration and associated cancer. Our ultimate goal is to identify novel ways to better treat or prevent childhood inflammatory bowel disease.CHLA-Polk-Lab-Colonoscopy-Epithelium.JPG

Our current areas of investigation include epidermal growth factor and tumor necrosis factor receptor signaling mechanisms leading to cellular growth, survival, development, wound healing and how these factors influence inflammation and cancer.

We have identified how these signaling systems contribute to disease in colitis models and how they influence long-term cancer risk, which is a major concern for pediat

ric patients with inflammatory bowel disease as they become adults with IBD.

Our goal is to better understand how to treat or prevent intestinal inflammation, injury and cancer.We hav

e also identified one of the only known mechanisms through which probiotic bacteria can protect the colon from injury and inflammation.

We use cutting-edge techniques to study these questions, including in vivo models, novel genetic approaches, cell culture systems, state-of-the-art microscopy and colonoscopy imaging systems.




Key Findings and Achievements

  • Determined the mechanisms controlling EGFR and TNFR1/2 signaling in colon epithelial cells.
  • Determined the roles of ErbB2 and ErbB3 in colitis.
  • Determined how the signaling molecule KSR regulates colon epithelial cell survival.
  • Identified and determined how a protein produced by probiotic bacteria protects colon epithelial cells and treats colitis.
  • Developed imaging technique to study intact colon at the molecular level

Current Funding


My laboratory is focused on the regulation of growth and development of the intestinal cell as it relates to growth, development and disease. Current areas of investigation include epidermal growth factor and tumor necrosis factor receptor family member signaling mechanisms leading to proliferation, differentiation, survival or migration of intestinal cells and the relationship between inflammation and tumorigenesis.

  • NIH R01DK056008: Cytokine regulation of intestinal epithelial restitution
    These studies are designed to test the hypothesis that during acute injury and chronic inflammation TNF stimulates TNFR processing and signal transduction, including transactivation of EGFR/ErbB2, to promote epithelial cell monolayer integrity and health of the host. The overall goal of these studies is to better understand the role of TNFR signaling during intestinal epithelial injury repair responses and inflammation.
  • NIH R01DK066176: Mechanism of KSR regulation of intestinal cell survival
    The goal of this proposal is to test our hypothesis that KSR kinase activity regulates IEC survival during the inflammatory response through activation of anti-apoptotic signal transduction pathways. Aim 1 is designed to determine the mechanisms regulating KSR activation. The focus of Aim 2 is to identify substrates and downstream targets of KSR in IECs. In Aim 3 we will study the biological role of KSR in intestinal epithelial injury using in vivo models.
  • NIH P01CA116087: H.pylori-induced inflammation and gastric cancer
    The overarching objective of Project 2 is delineation of the EGFR molecular signaling events initiated by H. pylori epithelial cell contact that regulate phenotypes related to gastric carcinogenesis.
  • Welcome Trust: The Role of NF-kB and Cell Shedding in Inflammatory Bowel Disease
    The goal of this proposal is to use models of IBD to identify molecular pathways that regulate gastrointestinal epithelial barrier function and bacterial translocation in chronic intestinal inflammation, with emphasis on the TNF and NF- kappaB signaling pathways.

Children's Hospital Los Angeles

4650 Sunset Blvd.
MS #71
Los Angeles, CA 90027
Phone: 323-361-2278Office
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