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© Perrine Bomme, Guillaume Duménil, Jean-Marc Panaud.
Coloured scanning electron micrograph (SEM) of Neisseria meningitidis on epithelial cells
Publication : PLoS pathogens

Hyperinvasive Meningococci Induce Intra-nuclear Cleavage of the NF-κB Protein p65/RelA by Meningococcal IgA Protease.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in PLoS pathogens - 04 Aug 2015

Besbes A, Le Goff S, Antunes A, Terrade A, Hong E, Giorgini D, Taha MK, Deghmane AE,

Link to Pubmed [PMID] – 26241037

Link to DOI [DOI] – 10.1371/journal.ppat.1005078

PLoS Pathog 2015 Aug; 11(8): e1005078

Differential modulation of NF-κB during meningococcal infection is critical in innate immune response to meningococcal disease. Non-invasive isolates of Neisseria meningitidis provoke a sustained NF-κB activation in epithelial cells. However, the hyperinvasive isolates of the ST-11 clonal complex (ST-11) only induce an early NF-κB activation followed by a sustained activation of JNK and apoptosis. We show that this temporal activation of NF-κB was caused by specific cleavage at the C-terminal region of NF-κB p65/RelA component within the nucleus of infected cells. This cleavage was mediated by the secreted 150 kDa meningococcal ST-11 IgA protease carrying nuclear localisation signals (NLS) in its α-peptide moiety that allowed efficient intra-nuclear transport. In a collection of non-ST-11 healthy carriage isolates lacking NLS in the α-peptide, secreted IgA protease was devoid of intra-nuclear transport. This part of iga polymorphism allows non-invasive isolates lacking NLS, unlike hyperinvasive ST-11 isolates of N. meningitides habouring NLS in their α-peptide, to be carried asymptomatically in the human nasopharynx through selective eradication of their ability to induce apoptosis in infected epithelial cells.

https://pubmed.ncbi.nlm.nih.gov/26241037