Distribution of enteric glia and GDNF during gut inflammation

BMC Gastroenterology

Research Article

Martin Steinkamp¹  Carolin Pflüger²  Ulrike Spaniol²  Georg BT von Boyen²  Nadine Schulte²  Christoph Hartmann² 

[1] Department of Gastroenterology, Endocrinology and Metabolism, University of Marburg, Marburg, Germany;Department of Medicine I (Gastroenterology), University of Ulm, Ulm, Germany;

关键词: Ulcerative Colitis;    Glial Fibrillary Acidic Protein;    Ulcerative Colitis Patient;    Glial Fibrillary Acidic Protein Expression;    Inflame Colon;   

DOI  :  10.1186/1471-230X-11-3

 received in 2010-10-06, accepted in 2011-01-14,  发布年份 2011

来源: Springer

【 摘 要 】

BackgroundThe enteric glia network may be involved in the pathogenesis of inflammatory bowel disease (IBD). Enteric glia cells (EGCs) are the major source of glial-derived neurotrophic factor (GDNF), which regulates apoptosis of enterocytes. The aim of the study was to determine the distribution of EGCs and GDNF during gut inflammation and to elucidate a possible diminished enteric glia network in IBD.MethodsThe expression of glial fibrillary acidic protein (GFAP) in colonic biopsies of patients with IBD, controls and patients with infectious colitis was detected by immunohistochemistry and Western blot. Tissue GDNF levels were measured by ELISA.ResultsThe expression of GFAP and GDNF in the mucosal plexus is highly increased in the inflamed colon of patients with ulcerative colitis (UC) and infectious colitis. Although the GDNF and GFAP content are increased in Crohn's disease (CD), it is significantly less. Additionally the non-inflamed colon of CD patients showed a reduced GFAP and no GDNF expression compared to controls and the non-inflamed colon of UC patients.ConclusionsGFAP and GDNF as signs of activated EGCs are increased in the inflamed mucosa of patients with UC and infectious colitis, which underline an unspecific role of EGC in the regulation of intestinal inflammation. The reduced GFAP and GDNF content in the colon of CD patients suggest a diminished EGC network in this disease. This might be a part of the pathophysiological puzzle of CD.

【 授权许可】

CC BY   
© von Boyen et al; licensee BioMed Central Ltd. 2011