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The Korean Association of Immunobiologists (대한면역학회)
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Granulocyte Colony Stimulating Factor (G-CSF) Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis in Mice

마우스 염증성 장 질환 모델에서 G-CSF (Granuocyte Colony Stimulating Factor)에 의한 염증 완화

  • 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)
  • 최은영 (경북대학교 의과대학 생리학교실) ;
  • 전창덕 (경북대학교 의과대학 생리학교실) ;
  • 오재민 (원광대학교 의과대학 해부학교실) ;
  • 김유림 (원광대학교 의과대학 해부학교실) ;
  • 이수택 (전북대학교 의과대학 소화기내과) ;
  • 김상욱 (전북대학교 의과대학 소화기내과)
  • Published : 2006.03.30
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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

References

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