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Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
Published on: May 21, 2012
Elevation of interleukin-6 in inflammatory bowel disease is macrophage- and epithelial cell-dependent
K Kusugami1, A Fukatsu, M Tanimoto
1First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Insights
Elevated local interleukin-6 (IL-6) activity is a key feature of active inflammatory bowel disease (IBD). Macrophages and colonic epithelial cells are the primary sources of this increased IL-6 in active IBD patients.
Area of Science:
- Gastroenterology
- Immunology
- Molecular Biology
Background:
- Inflammatory bowel disease (IBD) involves chronic inflammation of the digestive tract.
- Interleukin-6 (IL-6) is a cytokine implicated in inflammatory processes.
Purpose of the Study:
- To investigate local interleukin-6 (IL-6) activity in colonic tissues of patients with inflammatory bowel disease (IBD).
- To identify the cellular sources of IL-6 in active IBD.
Main Methods:
- Culturing of lamina propria mononuclear cells (LPMC) and colonic mucosal tissues.
- Northern blot analysis for IL-6 messenger RNA detection.
- Immunofluorescent microscopy for IL-6 protein localization.
Main Results:
- Active IBD specimens showed significantly higher IL-6 activity compared to controls.
- IL-6 messenger RNA and protein were detected in LPMC and colonic epithelial cells from active IBD patients.
- Increased IL-6-producing cells were observed in active IBD mucosal tissues.
Conclusions:
- Elevated local IL-6 activity is a characteristic feature of active IBD.
- Macrophages (CD68+ cells) and colonic epithelial cells are major contributors to IL-6 production in active IBD.
Abstract:
Local interleukin-6 (IL-6) activity was studied using colonic mucosal tissues in inflammatory bowel disease (IBD) and inflammatory control patients. Active IBD specimens exhibited significantly higher IL-6 activity than control specimens in both cultures of isolated lamina propria mononuclear cells (LPMC) and mucosal tissues with an increased number of IL-6-producing cells. However, the activity in inactive IBD or inflammatory controls did not differ from controls. Northern blot analysis demonstrated IL-6 messenger RNA in LPMC and colonic epithelial cells isolated from active IBD specimens but not in control cells. Furthermore, immunofluorescent microscopic study of active IBD specimens showed more conspicuous staining of IL-6 in infiltrating LPMC (mostly CD68+ cells) and colonic epithelial cells. These results suggest that elevation of local IL-6 activity may be a characteristic feature of active IBD and both macrophages and colonic epithelial cells are the major cell types responsible for this phenomenon.
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