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491 results on '"Couraud, Pierre-Olivier"'

11. The use of a multicellular in vitro model to investigate uptake and migration of bacterial extracellular vesicles derived from the human gut commensal Bacteroides thetaiotaomicron.

Author

Modasia, Amisha A., Jones, Emily J., Martel, L. Marie-Pascale, Louvel, Hélène, Couraud, Pierre-Olivier, Blackshaw, L. Ashley, and Carding, Simon R.

Subjects
EXTRACELLULAR vesicles, TARGETED drug delivery, BACTEROIDES, CENTRAL nervous system, ENDOTHELIAL cells
Abstract

Bacterial extracellular vesicles (BEVs) are increasingly seen as key signalling mediators between the gut microbiota and the host. Recent studies have provided evidence of BEVs ability to transmigrate across cellular barriers to elicit responses in other tissues, such as the central nervous system (CNS). Here we use a combination of single-, two- and three-cell culture systems to demonstrate the transmigration of Bacteroides thetaiotaomicron derived BEVs (Bt-BEVs) across gut epitheliumand blood brain barrier (BBB) endothelium, and their subsequent acquisition and downstream effects in neuronal cells. Bt-BEVs were shown to traffic to the CNS in vivo after intravenous administration to mice, and in multi-cell in vitro culture systems to transmigrate across gut epithelial and BBB endothelial cell barriers, where they were acquired by both microglia and immature neuronal cells. No significant activation/inflammatory effects were induced in non-differentiated neurons, in contrast to that observed in microglia cells, although this was notably less than that induced by lipopolysaccharide (LPS). Overall, our findings provide evidence for transmigration of Bt-BEVs across gut-epithelial and BBB endothelial cell barriers in vivo and in vitro, and their downstream responses in neural cells. This study sheds light onto how commensal bacteria-derived BEV transport across the gut-brain axis and can be exploited for the development of targeted drug delivery. [ABSTRACT FROM AUTHOR]

Published
2023
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15. Methylphenidate-triggered ROS generation promotes caveolae-mediated transcytosis via Rac1 signaling and c-Src-dependent caveolin-1 phosphorylation in human brain endothelial cells

Author

Coelho-Santos, Vanessa, Socodato, Renato, Portugal, Camila, Leitão, Ricardo A., Rito, Manuel, Barbosa, Marcos, Couraud, Pierre-Olivier, Romero, Ignacio A., Weksler, Babette, Minshall, Richard D., Fontes-Ribeiro, Carlos, Summavielle, Teresa, Relvas, João B., and Silva, Ana P.

Published
2016
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24. Hepatitis C Virus Infects the Endothelial Cells of the Blood-Brain Barrier

Author

Fletcher, Nicola F., Wilson, Garrick K., Murray, Jacinta, Hu, Ke, Lewis, Andrew, Reynolds, Gary M., Stamataki, Zania, Meredith, Luke W., Rowe, Ian A., Luo, Guangxiang, Lopez–Ramirez, Miguel A., Baumert, Thomas F., Weksler, Babette, Couraud, Pierre–Olivier, Kim, Kwang Sik, Romero, Ignacio A., Jopling, Catherine, Morgello, Susan, Balfe, Peter, and McKeating, Jane A.

Published
2012
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30. Pathogenic Neisseria meningitidis utilizes CD147 for vascular colonization

Author

Bernard, Sandra C, Simpson, Nandi, Join-Lambert, Olivier, Federici, Christian, Laran-Chich, Marie-Pierre, Maïssa, Nawal, Bouzinba-Ségard, Haniaa, Morand, Philippe C, Chretien, Fabrice, Taouji, Saïd, Chevet, Eric, Janel, Sébastien, Lafont, Frank, Coureuil, Mathieu, Segura, Audrey, Niedergang, Florence, Marullo, Stefano, Couraud, Pierre-Olivier, Nassif, Xavier, and Bourdoulous, Sandrine

Published
2014
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33. Assessment of electrophile damage in a human brain endothelial cell line utilizing a clickable alkyne analog of 2-chlorohexadecanal

Author

Nusshold, Christoph, Üllen, Andreas, Kogelnik, Nora, Bernhart, Eva, Reicher, Helga, Plastira, Ioanna, Glasnov, Toma, Zangger, Klaus, Rechberger, Gerald, Kollroser, Manfred, Fauler, Günter, Wolinski, Heimo, Weksler, Babette B., Romero, Ignacio A., Kohlwein, Sepp D., Couraud, Pierre-Olivier, Malle, Ernst, and Sattler, Wolfgang

Published
2016
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42. Primary Angiitis of the Central Nervous System: Description of the First Fifty-Two Adults Enrolled in the French Cohort of Patients With Primary Vasculitis of the Central Nervous System

Author

de Boysson, Hubert, Zuber, Mathieu, Naggara, Olivier, Neau, Jean-Philippe, Gray, Françoise, Bousser, Marie-Germaine, Crassard, Isabelle, Touzé, Emmanuel, Couraud, Pierre-Olivier, Kerschen, Philippe, Oppenheim, Catherine, Detante, Olivier, Faivre, Anthony, Gaillard, Nicolas, Arquizan, Caroline, Bienvenu, Boris, Néel, Antoine, Guillevin, Loïc, and Pagnoux, Christian

Published
2014
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44. JAM-L-mediated leukocyte adhesion to endothelial cells is regulated in cis by [alpha]4[beta]1 integrin activation

Author

Luissint, Anny-Claude, Lutz, Pierre G., Calderwood, David A., Couraud, Pierre-Olivier, and Bourdoulous, Sandrine

Subjects
Cell adhesion molecules -- Chemical properties, Cell adhesion -- Research, Endothelium -- Chemical properties, Biological sciences
Abstract

Junctional adhesion molecules (JAMs) are endothelial and epithelial adhesion molecules involved in the recruitment of circulating leukocytes to inflammatory sites. We show here that JAM-L, a protein related to the JAM family, is restricted to leukocytes and promotes their adhesion to endothelial cells. Cis dimerization of JAM-L is required to engage in heterophilic interactions with its cognate counter-receptor CAR (cox-sackie and adenovirus receptor). Interestingly, JAM-L expressed on neutrophils binds CAR independently of integrin activation. However, on resting monocytes and T lymphocytes, which express the integrin VLA-4, JAM-L molecules engage in complexes with VLA-4 and mainly accumulate in their monomeric form. Integrin activation is required for the dissociation of JAM-L-VLA-4 complexes and the accumulation of functional JAM-L dimers, which indicates that the leukocyte integrin VLA-4 controls JAM-L function in cis by controlling its dimerization state. This provides a mechanism through which VLA-4 and JAM-L functions are coordinately regulated, allowing JAM-L to strengthen integrin-dependent adhesion of leukocytes to endothelial cells.

Published
2008

46. Neisseria meningitidis infection of human endothelial cells interferes with leukocyte transmigration by preventing the formation of endothelial docking structures

Author

Doulet, Nicolas, Donnadieu, Emmanuel, Laran-Chich, Marie-Pierre, Niedergang, Florence, Nassif, Xavier, Couraud, Pierre Olivier, and Bourdoulous, Sandrine

Subjects
Membrane proteins -- Research, Neisseria meningitidis -- Research, Biological sciences
Abstract

Neisseria meningitidis elicits the formation of membrane protrusions on vascular endothelial cells, enabling its internalization and transcytosis. We provide evidence that this process interferes with the transendothelial migration of leukocytes. Bacteria adhering to endothelial cells actively recruit ezrin, moesin, and ezrin binding adhesion molecules. These molecules no longer accumulate at sites of leukocyte-endothelial contact, preventing the formation of the endothelial docking structures required for proper leukocyte diapedesis. Over-expression of exogenous ezrin or moesin is sufficient to rescue the formation of docking structures on and leukocyte migration through infected endothelial monolayers. Inversely, expression of the dominant-negative N[H.sub.2]-terminal domain of ezrin markedly inhibits the formation of docking structures and leukocyte diapedesis through noninfected monolayers. Ezrin and moesin thus appear as pivotal endothelial proteins required for leukocyte diapedesis that are titrated away by N. meningitidis. These results highlight a novel strategy developed by a bacterial pathogen to hamper the host inflammatory response by interfering with leukocyte-endothelial cell interaction.

Published
2006

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