Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis
dc.contributor.author | Kapoor, Kunal | |
dc.contributor.examiningcommittee | Uzonna, Jude (Immunology) Rastegar, Mojgan (Biochemistry and Medical Genetics) | en_US |
dc.contributor.supervisor | Ghia, Jean-Eric (Immunology) | en_US |
dc.date.accessioned | 2019-01-07T14:55:17Z | |
dc.date.available | 2019-01-07T14:55:17Z | |
dc.date.issued | 2018 | en_US |
dc.date.submitted | 2018-10-30T02:29:09Z | en |
dc.degree.discipline | Immunology | en_US |
dc.degree.level | Master of Science (M.Sc.) | en_US |
dc.description.abstract | Ulcerative colitis(UC) is characterized by a decreased level of chromofungin (CHR: Chormogranin-A 47-66) and a dysregulation of CD11c+ cells. We aimed to investigate the association between CHR and CD11c+ cells in an experimental model of UC. Colitis was induced in C57BL/6 mice by 5% dextran sulfate sodium with intra-rectal injection of CHR. Disease activity was monitored and colonic, mesenteric lymph node and splenic levels of pro-inflammatory cytokines and CD markers were assessed using ELISA and/or RT-qPCR. In-vivo, CHR treatment reduced colitis with a significant decrease in colonic levels of pro-inflammatory markers. In MLN, CHR decreased CD11c+ markers and in splenic CD11c+ cells CHR decreased CD40 and CD80. RT-2 PCR array demonstrated a downregulation of NF-kB in colon and in CD11c+ isolated cells from mice treated with CHR. NF-kB blocker/activator studies confirmed regulation by CHR. CHR regulates the development of colitis through the modulation of CD11c+ cells markers of immune activation. | en_US |
dc.description.note | February 2019 | en_US |
dc.identifier.uri | http://hdl.handle.net/1993/33622 | |
dc.language.iso | eng | en_US |
dc.rights | open access | en_US |
dc.subject | Ulcerative Colitis | en_US |
dc.title | Anti-inflammatory role of chromofungin, a chromogranin A-derived peptide, in the context of colitis | en_US |
dc.type | master thesis | en_US |