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BIOGRAPHY:
Dr. Cossart received her Ph.D. in biochemistry from the University
of Paris in 1977. Her postdoctoral research was conducted at the
Pasteur Institute. In 1998 she received the Richard Lounsberry Prize
and a Helena Rubenstein/UNESCO Award for Women in Science Leadership
and in 2000 the Swedish Society of Medicine awarded her the 2000 Louis
Pasteur Gold Medal. Dr. Cossart is an “Officier de l'Ordre du
Merite” of the French Legion of Honor, president of the Conseil
Scientifique of the Pasteur Insitute, a corresponding member of the
French Academy of Sciences, and a member of the French Conseil National
de la Science. She currently holds the titles of Professor and Head of
the Unité des Interactions Bactéries Cellules at the
Pasteur Institute of Paris. Her HHMI project is on the molecular and
cellular basis of the infection of the human bacterial pathogen
Listeria monocytogenes.
RESEARCH ABSTRACT SUMMARY:
Molecular and Cellular Basis of Listeria monocytogenes
Infection: New Aspects
Listeria monocytogenes is a food-borne pathogen responsible
for gastroenteritis, meningitis, septicemia, and abortions, with a
mortality rate of 30 percent. It has the capacity to cross three
barriers during infection (the intestinal barrier, the bloodbrain
barrier, and the feto-placental barrier). In all infected tissues,
Listeria is intracellular due to its capacity to survive in
phagocytic cells and also to invade and survive in nonphagocytic cells.
Once inside cells, bacteria escape from the internalization vacuole and
spread from cell to cell by using the now well-understood phenomenon of
actin-based motility. Through a combination of cell biology, genomic,
and in vivo approaches, as well as epidemiological data, our knowledge
of the infectious process is improving, highlighting the many
bacterial, mammalian, and environmental factors that control the
success of an infection. New findings concern new virulence genes such
as bsh, a gene encoding a bile salt hydrolase, an enzyme that so
far has been identified only in bacterial commensals and allows
Listeria to persist in the intestine; new regulatory mechanisms
controlling expression of virulence genes, for example, an RNA
thermosensor; new aspects of the cell biology of entry process, for
example, the involvement of myosinVIIA, an unconventional myosin, in
the internalin–E-cadherin interaction and of Wave and VASP in the
InlB-mediated cytoskeleton rearrangements; and new epidemiological and
histological data highlighting how Listeria crosses the
physiological barriers. A complete picture of the human disease is
emerging.
Photo: Kent Kallberg, Kallberg Studios
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