M Noguchi1, N Hiwatashi, Z X Liu, T Toyota. 1. Department of Gastroenterology, Sendai Shakaihoken Hospital, Sendai, Japan. noguchim@fd5.so-net.ne.jp
Abstract
BACKGROUND: Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-3 transmit a same signal needed for growth and activation in granulocytes and macrophages, because these receptors utilize a common beta chain. Little is known about growth factors for intestinal myeloid cells in lesions of inflammatory bowel disease (IBD). AIM: To find out whether GM-CSF is produced by the intestinal cells in IBD patients and controls. METHODS: We measured levels of GM-CSF, tumor necrosis factor (TNF), and IL-3 in the media of organ culture and lamina propria mononuclear cells (LPMCs) culture of colonic mucosa from the patients with IBD. Next, we have investigated GM-CSF production of colonic epithelial cell lines. RESULTS: Spontaneous secretion of GM-CSF was increased in inflamed mucosa, while secretion of IL-3 was not detected. Release of GM-CSF was enhanced in LPMCs from inflamed mucosa. Mucosal GM-CSF production was correlated to TNF-alpha production. Colonic epithelial cell line and T cell produced GM-CSF with superantigen stimulation. CONCLUSION: We revealed pivotal production of GM-CSF but not IL-3 in intestinal lesion of IBD. Increased secretion of GM-CSF might lead to chronic gut inflammation. Copyright 2001 S. Karger AG, Basel
BACKGROUND:Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin (IL)-3 transmit a same signal needed for growth and activation in granulocytes and macrophages, because these receptors utilize a common beta chain. Little is known about growth factors for intestinal myeloid cells in lesions of inflammatory bowel disease (IBD). AIM: To find out whether GM-CSF is produced by the intestinal cells in IBD patients and controls. METHODS: We measured levels of GM-CSF, tumor necrosis factor (TNF), and IL-3 in the media of organ culture and lamina propria mononuclear cells (LPMCs) culture of colonic mucosa from the patients with IBD. Next, we have investigated GM-CSF production of colonic epithelial cell lines. RESULTS: Spontaneous secretion of GM-CSF was increased in inflamed mucosa, while secretion of IL-3 was not detected. Release of GM-CSF was enhanced in LPMCs from inflamed mucosa. Mucosal GM-CSF production was correlated to TNF-alpha production. Colonic epithelial cell line and T cell produced GM-CSF with superantigen stimulation. CONCLUSION: We revealed pivotal production of GM-CSF but not IL-3 in intestinal lesion of IBD. Increased secretion of GM-CSF might lead to chronic gut inflammation. Copyright 2001 S. Karger AG, Basel
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