Granulocyte Colony Stimulating Factor (G-CSF) Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis in Mice.
- Author:
Eun Young CHOI
1
;
Chang Duk JUN
;
Jae Min OH
;
Yu Rim KIM
;
Soo Teik LEE
;
Sang Wook KIM
Author Information
- Publication Type:Original Article
- Keywords: G-CSF; inflammatory bowel diseases; inflammation; TNBS
- MeSH: Animals; Blood Cells; Colitis*; Colon; Colony-Stimulating Factors*; Endothelial Cells; Granulocyte Colony-Stimulating Factor; Granulocytes*; Hematopoiesis; Humans; Inflammation; Inflammatory Bowel Diseases; Injections, Intraperitoneal; Intercellular Adhesion Molecule-1; Interleukin-1beta; Mice*; RNA, Messenger; Tumor Necrosis Factor-alpha; Ulcer; Weight Loss
- From:Immune Network 2006;6(1):13-19
- CountryRepublic of Korea
- Language:Korean
- Abstract: BACKGROUND: Granulocyte colony stimulating factor (G-CSF) is known as a cytokine central to the hematopoiesis of blood cells and to modulate their cellular functions. Besides granulocytes and their precursors, monocytes/macrophages and endothelial cells are direct target cells of G-CSF action. G-CSF influences immune cells in an anti-inflammatory way. METHODS: To evaluate whether G-CSF has a potential for preventing or ameliorating diseases characterized by mucosal inflammation, we used a mouse model with trinitrobenzene sulfonic acid (TNBS)-induced inflammatory colitis. To the mice model G-CSF was administrated daily by intraperitoneal injection. Macroscopic evaluation and immunohistochemical analysis of colonic tissues were performed. RESULTS: Recombinant human G-CSF significantly inhibited LPS-induced TNF-alpha mRNA expression in THP-1 cells. As for in vivo relevance, G-CSF dramatically reduced the weight loss of mice, colonic damage, and mucosal ulceration that characterize TNBS colitis. Moreover, G-CSF suppressed the expression of tumor necrosis factor-alpha, interleukin-1beta, and intercellular adhesion molecule-1 in TNBS colitis. CONCLUSION: Current results demonstrate that G-CSF may be an effective agent for the treatment of diseases characterized by mucosal inflammation.
