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Am J Physiol Gastrointest Liver Physiol 292: G231-G241, 2007. First published January 19, 2006; doi:10.1152/ajpgi.00276.2005
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INFLAMMATION/IMMUNITY/MEDIATORS

Enteric glia inhibit intestinal epithelial cell proliferation partly through a TGF-beta1-dependent pathway

M. Neunlist,1,* P. Aubert,1,* S. Bonnaud,2 L. Van Landeghem,1 E. Coron,1 T. Wedel,3 P. Naveilhan,4 A. Ruhl,5 B. Lardeux,1 T. Savidge,6 F. Paris,2 and J. P. Galmiche1

1INSERM U539, IMAD, University of Nantes, 44035 Nantes, France; 2INSERM U601, 44093 Nantes, France; 3Department of Anatomy, University of Luebeck, Luebeck, Germany; 4INSERM U643, 44093 Nantes, France; 5Technical University Munich, Department of Human Biology, Freising, Germany; 6Department of Gastroenterology, University of Texas Medical Branch, Galveston, Texas

Submitted 16 June 2005 ; accepted in final form 14 January 2006

Although recent studies have shown that enteric neurons control intestinal barrier function, the role of enteric glial cells (EGCs) in this control remains unknown. Therefore, our goal was to characterize the role of EGCs in the control of intestinal epithelial cell proliferation using an in vivo transgenic and an in vitro coculture model. Assessment of intestinal epithelial cell proliferation after ablation of EGCs in transgenic mice demonstrated a significant increase in crypt cell hyperplasia. Furthermore, mucosal glial network (assessed by immunohistochemical detection of S-100beta) is altered in colon adenocarcinoma compared with control tissue. In an in vitro coculture model of subconfluent Caco-2 cells seeded onto Transwell filters with EGCs, Caco-2 cell density and [3H]thymidine incorporation were significantly lower than in control (Caco-2 cultured alone). Flow cytometry analysis showed that EGCs had no effect on Caco-2 cell viability. EGCs induced a significant increase in Caco-2 cell surface area without any sign of cellular hypertrophy. These effects by EGCs were also seen in various transformed or nontransformed intestinal epithelial cell lines. Furthermore, TGF-beta1 mRNA was expressed, and TGF-beta1 was secreted by EGCs. Exogenously added TGF-beta1 reproduced partly the EGC-mediated effects on cell density and surface area. In addition, EGC effects on Caco-2 cell density were significantly reduced by a neutralizing TGF-beta antibody. In conclusion, EGCs have profound antiproliferative effects on intestinal epithelial cells. Functional alterations in EGCs may therefore modify intestinal barrier functions and be involved in pathologies such as cancer or inflammatory bowel diseases.

colon cancer; enteric nervous system


Address for reprint requests and other correspondence: M. Neunlist, INSERM U 539, Hôpital Hôtel Dieu, 1, place Alexis Ricordeau, 44035 Nantes, France (e-mail: michel.neunlist{at}univ-nantes.fr)






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