The C2 fragment fromNeisseria meningitidisantigen NHBA increases endothelial permeability by destabilizing adherens junctions
| Autor: | Riccardo Barrile, Marina de Bernard, Beatrice Aricò, Alessandro Casellato, Laura Ciucchi, Mariagrazia Pizza, Fleur Bossi, Gaia Codolo, Silvia Rossi Paccani |
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| Rok vydání: | 2014 |
| Předmět: |
Protease
medicine.diagnostic_test medicine.medical_treatment Proteolysis media_common.quotation_subject Neisseria meningitidis Immunology Biology Mitochondrion medicine.disease_cause medicine.disease Microbiology Adherens junction Sepsis Virology medicine Phosphorylation Internalization media_common |
| Zdroj: | Cellular Microbiology. 16:925-937 |
| ISSN: | 1462-5814 |
| DOI: | 10.1111/cmi.12250 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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