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Last update 2011-03-29 15:34:14.681

Michel Chignard Inate host defense and inflammation of the lungs

Course and current status


-Doctorat d'Etat from the University of Strasbourg (PhD) in 1977.


Present position:

-Director of Research at the Institut National de la Santé et de la Recherche Médicale (Inserm).

-Head of the Unit «Défense Innée et Inflammation», Institut Pasteur / Inserm U874, Paris, France.


Previous positions:

 - From June 15, 1973 to August 31, 1977

Pharmacologist, Merrell International Research Centre, Biochemical Pharmacology Unit, Strasbourg.

 - From September 1, 1977 to August 31, 1979

Assistant of Research, Institut Pasteur, Venom Unit, Department of Experimental Pathophysiology, 75015 Paris.

 - From September 1, 1979 to April 30, 1982

“Chargé de recherché”, Institut Pasteur, Venom Unit, Department of Experimental Pathophysiology, 75015 Paris.

 - From May 1, 1982 to August 1, 1985

Maître de recherche Inserm, Unité d'Immunopharmacologie de l'Allergie et de l'Inflammation, Inserm U 200, 92140 Clamart.

 - From August 1, 1985 to August 13, 1986

Visiting scientist at the Thrombosis Research Centre, Temple University School of Medicine, Philadelphia (Pr J.B. Smith).

 - From August 1986, to July 2001.

Leader of the research group «Cellular Interactions in Inflammation», Unité de Pharmacologie Cellulaire, Institut Pasteur.

 - Since July 2001.

Head of the Institut Pasteur Unit «Défense Innée et Inflammation», Department of Infection & Epidémiologie

-Since January 2003

Head of the Inserm Team U874

Scientific summary

At the time of my first research in 1973, carried out at Merrel Dow, a pharmaceutical company in Strasbourg, I studied the interactions of arachidonic acid (AA) with blood platelets both in vitro and in vivo. I showed that a platelet aggregating catabolite of archidonic acid, thromboxane A2, could be formed without the observation of an aggregation and that this formation could be modulated by various pharmacological agents acting on cyclooxygenase, the involved enzyme. The obtained results constituted the basis of my thesis (7 original publications). I then joined the Pasteur Institute in 1977 where I continued this work (6 original publications). The study of the underlying mechanisms led me to show the implication of a phospholipase A2. In 1978, in collaboration with two other groups, I started two other subjects of research (i) the role of phospholipid methylation during the process of aggregation, and (ii) the synthesis of the PAF (a specific phospholipid bearing aggregating properties) during platelet activation by various agonists. These two studies were published in part in Nature (1979 and 1981, the first one being quoted 388 times). In parallel, I studied the implication of platelets and PAF in an experimental model of bronchoconstriction in the guinea-pig (work having produced several publications of which one is quoted 450 times). From 1982, I took the direction of a research group within the unit Inserm U200 in Clamart, and focusing my interest on  PAF-platelet interactions. In parallel to this basic research (18 publications), I led several projects of applied research through contracts with pharmaceutical companies on topics concerning anti-inflammatory and anti-thrombotic drugs. In 1985-1986, I spent one year at Temple University School of Medicine in Philadelphia (USA) where I started to develop an original subject concerning the interactions between neutrophils and platelets (publication in PNAS). The following year, I joined the unit of Cellular Pharmacology (Inserm partner) at the Pasteur Institute where I developed a group (Cellular interactions in inflammation) dedicated to the study of the interactions between neutrophils and the surrounding cells. From this date, my research was mainly centered on in vitro studies of the role of neutrophil proteases in lung inflammation (40 original publications). Then, as from 1998, I developed an experimental in vivo approach to study pulmonary inflammation (3 articles published, quoted between 30 and 57 times). Currently directing of the unit “Innate  Defense and Inflammation” created at the Pasteur Institute in July 2001 and recognized by Inserm since January 1, 2003, I direct more specifically projects on lung infection to study the innate defense of the host and its harmful counterpart, the inflammatory process. I thus implemented the development of models of bacterial (P. aeruginosa), viral (Influenza A) and fungic (A. fumigatus) lung infection with in vitro (cultures of primary cells and cell lines from human or murine origins) and in vivo (genetically invalidated and transgenic mice) approaches. These various models of infection constitute the specificity and the originality of the research which is undertaken in the unit. I more particularly study the role of receptors sensing the presence of pathogens and inducing a defense reaction, the Toll-like receptors (TLR). We have thus highlighted the paradoxical role of TLR3 (harmful and not protector) during flu infection, of TLR4 and 5 in the infection by P. aeruginosa and B. cenocepacia, and of TLR2 in invasive aspergillosis. In parallel, and in the continuity of the preceding years, I study the role of proteases at the level of the bronchoalveolar environment. On the whole, since the creation of the Inserm unit, I am co-authors of 46 original articles of which 20 have already been quoted between 20 and 228 times and of which 4 have been indexed in F1000 Biology and 1 in F1000 Medicine.

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