The C2 fragment from Neisseria meningitidis antigen NHBA increases endothelial permeability by destabilizing adherens junctions.
Cell Microbiol
; 16(6): 925-37, 2014 Jun.
Article
in En
| MEDLINE
| ID: mdl-24397470
ABSTRACT
Neisseria meningitidis is a human pathogen that can cause fatal sepsis and meningitis once it reaches the blood stream and the nervous system. Here we demonstrate that a fragment, released upon proteolysis of the surface-exposed protein Neisserial Heparin Binding Antigen (NHBA), by the bacterial protease NalP, alters the endothelial permeability by inducing the internalization of the adherens junction protein VE-cadherin. We found that C2 rapidly accumulates in mitochondria where it induces the production of reactive oxygen species the latter are required for the phosphorylation of the junctional protein and for its internalization that, in turn, is responsible for the endothelial leakage. Our data support the notion that the NHBA-derived fragment C2 might contribute to the extensive vascular leakage typically associated with meningococcal sepsis.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Permeability
/
Adherens Junctions
/
Endothelial Cells
/
Antigens, Bacterial
/
Neisseria meningitidis
Limits:
Humans
Language:
En
Journal:
Cell Microbiol
Journal subject:
MICROBIOLOGIA
Year:
2014
Type:
Article
Affiliation country:
Italy