Published December 30, 2009
| Version v1
Journal article
Breaking the wall: targeting of the endothelium by pathogenic bacteria
Contributors
Others:
- Centre méditérannéen de médecine moléculaire (C3M) ; Université Nice Sophia Antipolis (1965 - 2019) (UNS)-Institut National de la Santé et de la Recherche Médicale (INSERM)
- Hôpital l'Archet
- Microorganismes et Barrières de l'Hôte (Equipe avenir) ; Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)
- Université Paris Descartes - Paris 5 (UPD5)
- Pathogénie des infections systémiques (UMR_S 570) ; Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
- Institut Cochin (UMR_S567 / UMR 8104) ; Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)
- We are supported by institutional funding from INSERM. Research in the E.L. laboratory is also supported by a grant from the Agence Nationale de la Recherche (ANR; grant RPV07055ASA) and the Association pour la Recherche sur le Cancer (ARC; grant 3800). Research in the S.B. and X.N. laboratories is also funded by grants from ANR and ARC. is M.L. is also funded by Institut Pasteur, ANR and FRM.
Description
The endothelium lining blood and lymphatic vessels is a key barrier separating body fluids from host tissues and is a major target of pathogenic bacteria. Endothelial cells are actively involved in host responses to infectious agents, producing inflammatory cytokines, controlling coagulation cascades and regulating leukocyte trafficking. In this Review, a range of bacteria and bacterial toxins are used to illustrate how pathogens establish intimate interactions with endothelial cells, triggering inflammatory responses and coagulation processes and modifying endothelial cell plasma membranes and junctions to adhere to their surfaces and then invade, cross and even disrupt the endothelial barrier.
Abstract
International audienceAdditional details
Identifiers
- URL
- https://pasteur.hal.science/pasteur-04820966
- URN
- urn:oai:HAL:pasteur-04820966v1
Origin repository
- Origin repository
- UNICA