Christian Jobin

Christian Jobin

Associate Professor

Department of Medicine

Ph.D., Immunology, Microbiology
Universite Laval, Quebec, Canada

Biosketch [.pdf]

Department of Medicine, Division of Gastroenterology and Hepatology

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Research Interests:

  • Bacteria/host response
  • Innate signal transduction
  • Innate signal transduction

Research Synopsis:

The intestine poses an interesting conundrum.  It must peacefully cohabit with a sea of commensal bacteria (~100 trillion) and a high load of bacterial products but swiftly respond to the presence of pathogenic microorganisms that threaten its integrity.  This task is especially challenging due to the presence of an abundant and complex lymphoid intestinal system and a high number of immune cells. A major clinical consequence of deregulated bacteria/host interaction in the intestine is the development of inflammatory bowel diseases (IBD). In addition, a serious medical complication for patients suffering from IBD is the development of colitis-associated colon cancer.  As a product of our co-evolution with bacteria, a communication system has developed that allow us to regulate one another and to maintain homeostasis in the face of this potentially highly antigenic milieu. An integral part of the cross-talk that occurs between the human intestine and its resident microbiota is performed by innate bacterial sensors known as pattern recognition receptors (PRRs).  Two main classes of PRRs have been shown to regulate communication between the intestinal epithelium and the microbiota.  Toll-like receptors (TLRs) and Nod-like receptors (NLRs) serve to alert the host to the presence of bacteria in the extracellular and intracellular spaces respectively.  The long-term goal of our research is to define the molecular mechanism regulating bacteria/host interaction in the intestine. Using mice housed in germ-free conditions and tissue specific gene deleted mice (immune and epithelial specific deletion), we study the cellular contribution of TLR- and NLR-derived signaling on bacteria-induced colitis, intestinal injury (ischemia/reperfusion) and colitis-associated colon cancer.  A classical effector system involved in the inflammatory, cancer and immune response is the NF-kB signaling cascade.  Our research program utilize various NF-kB gene reporter animals (IL-10-/-; NF-kBEGFP mice, NF-kBEGFP mice and Tg(NFKB:EGFP) zebrafish) to define the impact of bacteria on intestinal homeostasis and to identify compounds modulating NF-kB activity (EGFP expression) in vivo.

Publications:

pubmed

Click above for PubMed publications.

  • Uronis, J., and Jobin, C. (2009) Microbes and Colorectal Cancer:  Is There a Relationship?  Current Oncol 16(4):22-4. Abstract
  • Kim, J-Y., Kajino-Sakamoto, R.,  Omori, E., Jobin, C., and Ninomiya-Tsuji, J. (2009) intestinal epithelial-derived TAK1 signaling is essential for cytoprotection against chemical-induced colitis. PloS ONE. 4(2): e4561. Abstract
  • Joo, Y-E., Karrasch, T., Narula, A., Allard, B., Herfarth, H.H., and Jobin, C. (2009) Tomato lycopene extract prevents lipopolysaccharide-induced NF-kB signaling and gene expression, but worsens dextran sulfate sodium-induced colitis in transgenic NF-kBEGFP mice. PloS ONE.  4(2): e4562. Abstract
  • Kajino-Sakamoto, R., Inagaki, M., Lippert, E., Akira, S., Robine, S., Matsumoto, K., Jobin, C., and Ninomiya-Tsuji, J. (2008) Intestinal epithelial-derived TAK1 signaling prevents TNF-dependent intestinal damage and the development of ileitis and colitis. J. Immunol. 181(2): 1143-52. Abstract
  • Jobin, C. (2008) The NF-kB signaling cascade and IBD:  Turn it down? Inflamm. Bowel. Dis. 14(S2): S108-S109. Article
  • Karrasch, T., and Jobin, C. (2008) NF-kB in the intestine:  Friend or foe? Inflamm. Bowel. Dis. 14 (1): 114-24. Abstract
  • Mühlbauer M., Chilton P.M., Mitchell T.C., and Jobin C. (2008) Impaired Bcl3 up-regulation leads to enhanced LPS-induced IL-23p19 gene expression in IL-10-/- mice.  J. Biol. Chem. 283(21): 14182-9. Abstract
  • Karrasch T, Kim, J.S., Mühlbauer, M. Magness, S.T., and Jobin C. (2007) Gnotobiotic IL-10-/-;NF-kBEGFP mice reveal the critical role of TLR/NF-kB signaling in commensal bacteria-induced colitis. J. Immunol. 178 (10): 6622-6532. Abstract
  • Karrasch T, Kim, J.S., Byunk, I.J. and Jobin C. (2007) The flavonoid luteolin worsens chemical-induced colitis in NF-kBEGFP transgenic mice through blockade of enterocyte-derived NF-kB-dependent protective molecules. PloS ONE. Jul 4;2:e596. Abstract
  • Karrasch T, Steinbrecher K, Allard B, Baldwin, A.S. and Jobin C. (2006) Critical role for H3 phosphorylation and p38-MAPK pathway in intestinal wound-healing response J. Cell. Physiol. 207(3): 809-15. Abstract

Contact Information


Office Location:
7341-B Medical Biomolecular Research Bldg.
111 Mason Farm Rd.

Mailing Address:
CB # 7032
UNC-CH Dept. of Medicine
Chapel Hill, NC 27599-7032

Office Phone: 919-966-7884
Lab Phone: 919-843-6915
Fax: 919-843-6899
job[at]med.unc.edu

 

 

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