Alain Vandewalle
  • E-mail :[email]
  • Phone : +33 1 57 27 75 50
  • Location : Paris, France
Last update 2011-04-07 11:35:29.086

Alain Vandewalle Renal Epithelial cells and Inflammation

Course and current status

 Civil State: Vandewalle Alain , January 7th 1947, French

MD (1978) Nephrologist, PhD (1984)

Position:Research Director (DR1) at INSERM

Head of the Research group "Renal Epithelial Cells and Inflamation" at INSERM U773 (Director, Dr M. Laburthe)

Address: INSERM U773, Centre de Recherche Biomédicale Bichat Beaujon, Paris 75890, Paris, Cedex 18, Fr

Member of the ITMO Institute "Circulation, Metabolism and Nutrition"  (Director C. Boitard)

Member of the Scientific Council of the Faculty of Medicine (UFR) Paris

Expertise : Cell Biology, Renal pathophysiology, Toxicology, Inflammation.  sociétés savantes, conseils d’administration

Scientific summary

Epithelial cells lining the renal tubule, can be serevely injured in a variety of inflammatory disorders. Renal epithelial cells, like circulating immune cells, express a variety of Toll-like receptors (TLRs) and Nod-like receptors (NLRs), and participate to the initiation of the innate immune response. The main research theme of the group is to understand the role of renal tubule cells in the development of inflammatory response in pathophysiological situations affecting kidneys, particularly during ascending urinary tract infection (UTI) and ischemia reperfusion injury (IRI). We demonstrated that collecting duct cells are a preferential intrarenal site of adhesion and invasion of uropathogenic E. Coli (UPECs), and identified a novel hormonal regulatory pathway controlled by arginine vasopressin regulating innate immunity in kidneys infected with UPEC (Chassin et al. J Exp Med, 2007). UTI represent the main infectious complication of renal transplant recipients, but the mechanism Urinary tract infections (UTIs), mainly due to uropathogenic Escherichia coli (UPEC), are frequent infectious complications in renal transplant recipients under immunosuppressive treatment. However, it remains unclear how immunosuppressive drugs, such as the calcineurin inhibitor cyclosporine A, decrease the resistance to UPEC. Clinical and experimental studies are in progress to analyze the effects of CsA on the innate immune response of renal transplant recipients (Contrat Hospitalier de Recherche Translationnelle, 2010). IRI causes inflammation and parenchymal cell injury as a result of activating innate immune signaling, mainly mediated by TLR2 and TLR4. We have identified two key regulatory molecules, the protein phosphatase 5 and the NADPH oxidase 4 (NOX4), controlling TLR2- and TLR4-mediated activation of renal tubule cell apoptosis during IRI, respectively, which represent potential targets for new pharmacological strategies aimed to reduce apoptosis during IRI (Ben Mkaddem et al. J Biol Chem, 2009, Cell Death Differ, 2010).

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