Frédérick Barreau

Keywords: Environmental factors, Intestinal epithelium physio(patho)logy, Regeneration, , Intestinal permeability, Inflammation

Research programs

The intestinal epithelium represents an essential functional barrier for our body, enabling the absorption of nutrients, salts, and water while providing protection against pathogens. To fulfill these functions, the cells of the intestinal mucosa renew every 5 days, subjecting the digestive tract to significant stress in controlling proliferation, differentiation, and cellular organization. Intestinal renewal is tightly regulated and depends on the spatial organization of signals from supporting mesenchymal cells, particularly the fibroblasts that sheath the crypt and sustain the intestinal epithelium.

The homeostasis—and thus the integrity—of the intestinal epithelium is constantly challenged by external environmental factors from the intestinal lumen (food additives, nutritional compounds, microbiota, etc.) and internal factors (stroma, genetic predisposition, etc.). Environmental factors that promote or worsen colonic inflammation or disrupt epithelial cell renewal are a major concern. Indeed, any disruption of intestinal homeostasis contributes to the development of chronic inflammatory bowel diseases (IBD) and tumor transformation.

The two main forms of IBD are Crohn’s disease (CD) and ulcerative colitis (UC). One of the major complications of IBD is colorectal cancer (CRC). Additionally, sporadic colorectal cancer is the third leading cause of cancer-related mortality in industrialized countries.

Our research projects aim to investigate the impact of environmental factors—both external and internal—on the physio(patho)logy of the intestinal epithelium, the development of inflammatory processes, and carcinogenesis.

Membres

Arthur Mauduit
PhD Student

Emmanuel Mas
PU-PH

Frédérick Barreau
Researcher

Lisa Isoard
PhD Student

Sandrine Ménard
Researcher

Stéphanie Cassant-Sourdy
Staff

Cellular and Animal Models

Cellular Models

• Primary cultures of human colorectal fibroblasts
• Human and murine 3D colonic organoid primary cultures
• Caco-2 cells stably transfected with wild-type Nod2 or mutated polymorphisms
• Caco-2 cells stably transfected with 300A or 300T variants for ATG16L1

Animal Models

• Murine model of colorectal cancer: Orthotopic grafting in murine models
• Alterations in Nod2 pathways (Nod2 knockout or mutated mice)
• Alterations in endoplasmic reticulum stress pathways (IL-1 and NOX-1 knockout mice)

Methods

• 2D and 3D cell culture
• Animal experimentation
• Protein expression analysis (Western blot, etc.)
• RT-qPCR
• Capillary electrophoresis
• Confocal and two-photon imaging

Publications