Defective response to bacteria through lectin-type receptors in dendritic cells from Crohn diseases

2007 Fiscal Year Final Research Report Summary

• Project/Area Number: 18590701
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Keio University
• Principal Investigator: OKAMOTO Susumu Keio University, School of Medicine, Assistant Professor (70255446)
• Project Period (FY): 2006 – 2007
• Keywords: Crohn / dendritic cells / lectin / sugar chain

Research Abstract

Human peripheral blood monocytes were differentiated into three types of cells, that is, M-CSF-derived macrophages, GM-CSF-macophages, and dendritic cells. First we compared surface markers on these cells among normal controls (NL), ulcerative colitis (UC), and Crohn's disease (CD) patients, but could not demonstrate any difference in DC-SIGN (CD209), CD14, CD33, CD80, CD86, CD83, HLA-DR, CD206. Next, we stimulated these cells to measure cytokines with LPS and/or DC-SIGN ligands such as mannnann, zymosan, and laminarin. Dendritic cells tended to produce more IL-12 and IL-23, but there were no difference with statistical significance among NL, UC, and CD. Some previous reports demonstrated that DC-SIGN ligands could suppress the production of pro-inflammatory cytokines from LPS-stimulated macrophages. However, I could not see the suppressive effect of DC-SIGN ligands in this set of experiments and now I am trying to find optimal conditions.