Hansen, Jonathan



Education and Training 

Degree Institution Area
BS Brigham Young University Biochemistry
MD Indiana University School of Medicine Medicine
PhD Indiana University School of Medicine Microbiology & Immunology
Residency University of North Carolina Internal Medicine
Fellowship University of North Carolina Gastroenterology & Hepatology
Post-doctoral Research Fellowship University of North Carolina Host-microbial interactions
Clinical Interests

 "Dr. Hansen's clinical practice is devoted to the care of patients with simple and complicated inflammatory bowel diseases including Crohn's disease, ulcerative colitis, microscopic colitis, and other immune-mediated intestinal diseases.  He is a sub-investigator on numerous inflammatory bowel disease clinical research trial protocols at UNC."


       Center for Gastrointestinal Biology and Diseases Research Competition, 1st place, 2007
2.       Chairman’s Award—Internal Medicine, University of North Carolina at Chapel Hill, 2005.
3.       John B. Hickam Award for high standards of performance in internal medicine, 2003.
4.       Member of Alpha-Omega-Alpha Medical Honor Society, 2002-2003
5.       Indiana Medical Scientist Training Program Fellowship, Indiana University School of Medicine, 1996-2003.
6.       Chancellor's Scholar Award Nominee, Indiana University-Purdue University at Indianapolis, 2002.
7.       Dr. Karl R. Ruddell Scholarship, Walther Cancer Institute, Indianapolis, IN, 1999.
8.       Gene Therapy Research Fellowship, Indiana University School of Medicine, 1998-1999.
9.       Merit Scholarship, Indiana University School of Medicine, 1996-1997.


Research Interests

Current research indicates that inflammatory bowel diseases (IBD’s), including Crohn’s disease and ulcerative colitis, are due to uncontrolled innate and adaptive immune responses to commensal intestinal bacteria in genetically susceptible hosts.  The role of bacteria in the pathogenesis of IBD’s is highlighted by genome-wide association studies that have identified 12 IBD susceptibility loci that overlap with those for mycobacterial infections (Jostins et al., Nature 2012).  Furthermore, in virtually all animal models of IBD tested to date, the presence of intestinal bacteria is necessary for the development of intestinal inflammation.

While it is becoming increasingly clear how commensal (non-pathogenic) intestinal bacteria initiate the chronic T-cell mediated intestinal inflammation observed in IBD’s and experimental colitis, their roles in the perpetuation and progression of disease is unclear.  Moreover, the effects of host inflammation on commensal bacterial physiology and virulence are unknown.  We hypothesize that commensal bacteria dynamically respond to intestinal inflammation in a manner that perpetuates or worsens disease.  For instance, bacterial antigens and adjuvants initiate intestinal inflammation, which in turn leads to the production of mediators including reactive oxygen species, inflammatory cells, and cytokines that consequently enhance the growth and virulence of the bacteria.


Exploring this hypothesis will enhance our understanding of the pathogenesis of IBD’s and host-microbial interactions, and potentially identify new therapeutic targets for these currently incurable diseases.

Our lab focuses on the following main projects:

1)      Identification of inflammation-associated transcriptional responses in commensal intestinal bacteria during experimental colitis that impact the course of disease.  We use a combination of gnotobiotic (defined microbial environment) technology in mice, molecular biology, bacterial mutagenesis, dietary interventions, microarrays, microbial RNA-Seq, and ex-vivo immune cell assays to identify bacterial genes that are differentially expressed during inflammation and mechanisms of how these genes affect host immune responses.

2)      Characterize how experimental colitis impacts the genetic microevolution of commensal intestinal bacteria.  We use gnotobiotic technology in mice, next generation bacterial genome sequencing, bacterial mutagenesis, high throughput bacterial phenotyping assays, and redox chemistry to identify genetic mutations that accumulate in bacteria during colitis, characterize their effect on protein function and bacterial physiology, and ultimately how mutations affect the growth and virulence of commensal bacteria during experimental colitis.

Link to list of publications on PubMed.

(O) 919-843-5854
(F) 919-843-6899


Clinical Interests