Granulocyte Colony Stimulating Factor (G-CSF) Attenuates 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-induced Colitis in Mice
Immune Network
; : 13-19, 2006.
Article
de Ko
| WPRIM
| ID: wpr-109770
Bibliothèque responsable:
WPRO
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.
Mots clés
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Ulcère
/
Cellules sanguines
/
ARN messager
/
Maladies inflammatoires intestinales
/
Perte de poids
/
Facteur de stimulation des colonies de granulocytes
/
Facteurs de stimulation des colonies
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Facteur de nécrose tumorale alpha
/
Colite
/
Côlon
Type d'étude:
Prognostic_studies
Limites du sujet:
Animals
/
Humans
langue:
Ko
Texte intégral:
Immune Network
Année:
2006
Type:
Article