Publications by authors named "Chakir Bello"
Article Synopsis
- Vinculin is a protein that helps cells stick together, and the IpaA invasion effector enhances its activity by promoting a unique protein structure called supra-activation, which aids in cell adhesion.
- The study focused on specific mutations in vinculin's subdomains that interact with IpaA, revealing that these mutations influenced the formation of vinculin trimers and how quickly monomers disappeared.
- Results showed that certain mutations decreased the ability of cells to be invaded, indicating that IpaA's role is more about enhancing cell-matrix adhesion rather than facilitating bacterial invasion, as confirmed by experiments on shear stress effects.
Pneumococcal (PN) meningitis is a life-threatening disease with high mortality rates that leads to permanent neurological sequelae. Studies of the process of bacterial crossing of the blood brain barrier (BBB) are hampered by the lack of relevant and models of meningitis that recapitulate the human disease. PN meningitis involves bacterial access to the bloodstream preceding translocation across the BBB.
View Article and Find Full Text PDFStreptococcus pneumoniae or pneumococcus (PN) is a major causative agent of bacterial meningitis with high mortality in young infants and elderly people worldwide. The mechanism underlying PN crossing of the blood brain barrier (BBB) and specifically, the role of non-endothelial cells of the neurovascular unit that control the BBB function, remains poorly understood. Here, we show that the astroglial connexin 43 (aCx43), a major gap junctional component expressed in astrocytes, plays a predominant role during PN meningitis.
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