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Sean P. Colgan

Ph.D., Director of Mucosal Inflammation Program



Contact Info:

Molecular Biology
University of Colorado

Sean Colgan, Ph.D.  Research Two
(RC2) Room 10025 Phone: 303-724-7235



  • Undergraduate: BS, Microbiology, Colorado State University, Fort Collins, CO
  • Graduate:
    • MS, Experimental Pathology, Colorado State University, Fort Collins, CO
    • PhD, Experimental Pathology, Colorado State University, Fort Collins, CO
  • Research Fellowship: Harvard Medical School

Honors and Awards

  • 1994 - Society of Leukocyte Biology: Young Investigator Award
  • 1999 - Mark and Diane Goldman and Family Research Scholar
  • 1999 - Designated Lecture, Physiological Society, Newcastle, UK
  • 2006 - Honorary M.A.: Harvard University, Cambridge, MA
  • 2008 - University of Colorado Outstanding PhD Research and Teaching Award
  • 2010 - R37 MERIT (Method to Extend Research in Time) Award, NIH - National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK).

Faculty Appointments

  • 1994 - Instructor, Harvard Medical School
  • 1994 - 1999 - Assistant Professor, Harvard Medical School
  • 1999 - 2005 - Associate Professor, Harvard Medical School
  • 2005 - 2006 - Professor, Harvard Medical School
  • 2006 - present - Levine-Kern Professor of Medicine, University of Colorado Denver
  • 2006 - present - Director, Mucosal Inflammation Program, University of Colorado Denver
  • 2010 - Professor of Immunology, University of Colorado
  • 2011 - Vice Chair for Research, Department of Medicine, University of Colorado

Committees and Responsibilities

  • 2007 - 2010 Member, General Medicine and Pathobiology (GMPB) Study Section, NIH - NIDDK
  • 2006 - Member, Crohn's & Colitis Foundation of America (CCFA) Medical Advisory Committee, Rocky Mountain Region
  • 2008 - Chairman, External Advisory Committee, Colorado Center for AIDS Research
  • 2006 - 2010 - Section Editor, Journal of Immunology
  • 2010 - 2012 - Chairman, GMPB Study Section
Studies from Dr. Colgan's laboratory are aimed at understanding how epithelial and endothelial cells coordinate inflammatory bowel disease.
  • Leukocyte cell-cell interactions: The pathological hallmark of many mucosal diseases is the accumulation of inflammatory cells such as neutrophils, macrophages and lymphocytes. At present, the signals and events which elicit recruitment of leukocytes to mucosal sites is not fully understood. Ongoing studies are aimed at determining the cellular and acellular components which contribute to trafficking of leukocytes across cell surfaces such as the intestine during infectious and inflammatory events. Specifically, we have focused on defining epithelial adhesion molecules important in neutrophil-epithelial interactions, and how such interactions might be regulated by soluble mediators present in the tissue microenvironment (chemokines, cytokines, lipids). Understanding the basic mechanisms of these events provide the basis for development of specific therapies aimed at treating such inflammatory conditions.
  • Regulation of epithelial structure/function during inflammation: Epithelial cells which line mucosal organs such as the lung and intestine provide a barrier and a conduit for vectoral fluid transport. Our laboratory has a particular interest in defining the regulation of structural features of epithelial cells (polarity, membrane ion channels, cytoskeletal elements) during inflammation. Recent studies, for example, indicate that during periods of modeled inflammation, epithelial cells lose many classic epithelial features (e.g. barrier function, ion secretion) and garner many qualities indicative of immune accessory cells (e.g. MHC class expression, chemokine/cytokine synthesis). This epithelial “phenotype switch” contributes to the pathophysiologic mechanisms of mucosal diseases such as inflammatory bowel disease (IBD) and cystic fibrosis, and current studies are directed at developing models to examine potential therapeutic approaches to treat such disorders.
  • Transcriptional signaling by hypoxia during inflammation: Diminished oxygen tension (hypoxia) is a contributing factor to developmental pathways and to a number of disease processes, including inflammation. Basic mechanisms of eukaryotic oxygen sensing and the transcriptional profile of genes induced by cellular hypoxia are not fully elucidated. Current studies are aimed at understanding basic cellular signaling pathways which contribute to transcriptional regulation of gene expression by hypoxia. Specifically, we employ the use of differential mRNA display technologies to profile transcriptional regulation of eukaryotic genes during episodes of diminished oxygen tension. Such studies are aimed at understanding novel crosstalk pathways between different cell types, how such crosstalk may be important during episodes of inflammation, and strategies for development of putative therapeutics.

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