Loic Guillot
  • E-mail :[email]
  • Phone : +33 1 49 28 46 82
  • Location : Paris, France
Last update 2011-08-26 10:13:58.953

Loic Guillot PhD

Course and current status

Sept 2010-

Researcher-Inserm UMR_S 938-Paris, FRANCE

PI: Pr. A. Clement

Sept 2007-Aug 2010

Postdoctoral fellow-Inserm UMR_S 938-Paris, FRANCE

PI: Pr. A. Clement

Jan 2005-June 2007

Postdoctoral fellow-McGill University-Centre for host resistance-Montreal, QC, CANADA

PI: Dr. S. Qureshi

http://meakins.mcgill.ca/qureshi.php

Oct 2004-Dec 2004

Postdoctoral Fellow-Pasteur Institute-Inserm-Innate Defense and Inflammation, Paris, FRANCE

PI: Dr. M. Chignard

Oct 2001-Oct 2004

PhD-Pasteur Institute-Inserm-Innate Defense and Inflammation, Paris, FRANCE

PI: Dr. M. Chignard

http://www.pasteur.fr/recherche/RAR/RAR2009/Defin-en.html

Scientific summary

I am working on diffuse lung disease in children, including interstitial lung disease (ILD) and chronic neonatal lung disease. It is a rare heterogeneous group of chronic disorders characterized by impaired gas exchange in the alveoli. These disorders classified in 2007 include ILD associated with surfactant genetic defects. Surfactant plays a critical role in the lung function. It stabilizes the alveoli during the respiratory cycle in preventing alveolar collapse at end expiration. Pulmonary surfactant is a multimolecular complex constituted of glycerophospholipids (~80%), cholesterol (~10%) and of 10 to 15% of proteins including 2 to 3 % of specific proteins called SP-A, SP-B, SP-C, and SP-D. The ATP-binding cassette, sub-family A, member 3 (ABCA3) protein is a transmembrane protein that play a critical role in the processing of surfactant. The synthesis of these proteins (SP-A, SP-B, SP-C, SP-D and ABCA3) is controlled by different transcription factors such as NK2 homeobox 1 (NKX2-1), also known as thyroid transcription factor 1 (TTF-1) and occurs in the endoplasmic reticulum (ER) of alveolar type II cells. The aim of my research program is to clarify the role of surfactant protein in the pathogenesis of ILD.

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