Christian Jobin, Ph.D.
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job@med.unc.edu
7341B MBRB 919.966.7884 |
Research
My research program focuses on an important medical problem: the pathological consequences of dysregulated immune host response to the intestinal commensal microbiota. A major clinical consequence of deregulated bacteria/host interaction in the intestine is the development of inflammatory bowel diseases (IBD). The economic burden for inflammatory bowel diseases (IBD) treatment is significant with costs in the United States estimated to be $6.3 billion. Using genetically engineered mice and zebrafish maintain in axenic condition, Dr. Jobin’s laboratory investigates the beneficial and pathological host responses to commensal and pathogenic microorganisms.
The research program is divided into three main thematics. 1) Role of bacteria and pattern recognition receptors in intestinal injury responses. Wound healing responses is studied in the context of ischemia/reperfusion and chemical (DSS, NSAIDs)-induced injury. 2) Interaction between bacteria, inflammation and development of colitis-associated colorectal cancer. A serious medical complication for patients suffering from IBD is the development of colitis-associated colon cancer. Using experimental model of colitis-associated colorectal cancer, we are investigating the relationship between the microbiota, inflammation and the development of colorectal cancer. 3) Molecular mechanism responsible for Campylobacter jejuni (C. jejuni) induced gastrointestinal illness. The Gram-negative invasive bacterium C. jejuni is the leading cause of bacterial food-borne gastrointestinal illness worldwide, with approximately 2-3 million annual cases in the United States alone. However, limited information is available on both host responses and the molecular mechanisms by which the microorganism triggers diseases. We have developed a model to C. jejuni induced pathogenesis that takes advantage of gnotobiotic technology. Our goal is to characterize the signaling events leading to C. jejuni) induced pathogenesis.
Publications
Goldsmith JR, Uronis JM, Jobin C (2011). Mu opioid signaling protects against acute murine intestinal injury in a manner involving stat3 signaling. Am J Pathol. 179(2):673-83
Gerhard Rogler G, Haller D, Jobin C (2011). Microbiota in chronic mucosal inflammation. Int J Inflam. 2010:395032.
Jobin C (2010). Probiotics and ileitis: could augmentation of TNF/NFκB activity be the answer? Gut Microbes. 1(3):196-9.
Jobin C (2010). MyD88 signaling in the intestine: Dr Jekyll and Mr Hyde? Gastroenterology. 139(2):383-5.
Uronis JM, Arthur JC, Keku T, Fodor A, Carroll IM, Cruz ML, Appleyard CB, Jobin C (2011). Gut microbial diversity is reduced by the probiotic VSL#3 and correlates with decreased TNBS-induced colitis. Inflamm Bowel Dis. 17(1):289-97. doi: 10.1002/ibd.21366.
Lippert E, Karrasch T, Sun X, Allard B, Herfarth HH, Threadgill D, Jobin C (2009). Gnotobiotic IL-10; NF-kappaB mice develop rapid and severe colitis following Campylobacter jejuni infection. PLoS One. 4(10):e7413.
Uronis JM, Mühlbauer M, Herfarth HH, Rubinas TC, Jones GS, Jobin C (2009). Modulation of the intestinal microbiota alters colitis-associated colorectal cancer susceptibility. PLoS One. 4(6):e6026.
Joo YE, Karrasch T, Mühlbauer M, Allard B, Narula A, Herfarth HH, Jobin C (2009). Tomato lycopene extract prevents lipopolysaccharide-induced NF-kappaB signaling but worsens dextran sulfate sodium-induced colitis in NF-kappaBEGFP mice. PLoS One. 4(2):e4562.
Jobin C (2008). Nf-kappa B signaling cascade and IBD: turn it down? Inflamm Bowel Dis. 14 Suppl 2:S108-9.
Mühlbauer M, Chilton PM, Mitchell TC, Jobin C (2008). Impaired Bcl3 up-regulation leads to enhanced lipopolysaccharide-induced interleukin (IL)-23P19 gene expression in IL-10(-/-) mice. J Biol Chem. 283(21):14182-9.
Mühlbauer M, Cheely AW, Yenugu S, Jobin C (2008). Regulation and functional impact of lipopolysaccharide induced Nod2 gene expression in the murine epididymal epithelial cell line PC1. Immunology. 124(2):256-64.
Karrasch T, Kim JS, Jang BI, Jobin C (2007). The flavonoid luteolin worsens chemical-induced colitis in NF-kappaB(EGFP) transgenic mice through blockade of NF-kappaB-dependent protective molecules. PLoS One. 2(7):e596.
Karrasch T, Kim JS, Muhlbauer M, Magness ST, Jobin C (2007). Gnotobiotic IL-10-/-;NF-kappa B(EGFP) mice reveal the critical role of TLR/NF-kappa B signaling in commensal bacteria-induced colitis. J Immunol. 178(10):6522-32.
Karrasch T, Steinbrecher KA, Allard B, Baldwin AS, Jobin C (2006). Wound-induced p38MAPK-dependent histone H3 phosphorylation correlates with increased COX-2 expression in enterocytes. J Cell Physiol. 207(3):809-15.
Kim JS, Jobin C (2005). The flavonoid luteolin prevents lipopolysaccharide-induced NF-kappaB signalling and gene expression by blocking IkappaB kinase activity in intestinal epithelial cells and bone-marrow derived dendritic cells. Immunology. 115(3):375-87.
Jijon HB, Madsen KL, Walker JW, Allard B, Jobin C (2005). Serum amyloid A activates NF-kappaB and proinflammatory gene expression in human and murine intestinal epithelial cells. Eur J Immunol. 35(3):718-26.
Hoentjen F, Sartor RB, Ozaki M, Jobin C (2005). STAT3 regulates NF-kappaB recruitment to the IL-12p40 promoter in dendritic cells. Blood. 105(2):689-96.
