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Granulocyte Colony Stimulating Factor (G-CSF) Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis in Mice  

Choi, Eun-Young (Department of Physiology, Kyungpook National University School of Medicine)
Jun, Chang-Duk (Department of Physiology, Kyungpook National University School of Medicine)
Oh, Jae-Min (Department of Anatomy, Wonkwang University School of Medicine)
Kim, Yu-Rim (Department of Anatomy, Wonkwang University School of Medicine)
Lee, Soo-Teik (Department of Internal Medicine, Chonbuk National University School of Medicine)
Kim, Sang-Wook (Department of Internal Medicine, Chonbuk National University School of Medicine)
Publication Information
IMMUNE NETWORK / v.6, no.1, 2006 , pp. 13-19 More about this Journal
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: Re combinant 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-$1{\beta}$, 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.
Keywords
G-CSF; inflammatory bowel diseases; inflammation; TNBS;
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