Back to Search
Start Over
A novel link between Campylobacter jejuni bacteriophage defence, virulence and Guillain-Barré syndrome
- Source :
- European Journal of Clinical Microbiology & Infectious Diseases, 32(2), 207. Springer Verlag, European Journal of Clinical Microbiology & Infectious Diseases, 32(2), 207-226. Springer-Verlag, European Journal of Clinical Microbiology and Infectious Diseases, 32(2), 207-226, European Journal of Clinical Microbiology and Infectious Diseases 32 (2013) 2
- Publication Year :
- 2013
-
Abstract
- Guillain-Barr, syndrome (GBS) is a post-infectious disease in which the human peripheral nervous system is affected after infection by specific pathogenic bacteria, including Campylobacter jejuni. GBS is suggested to be provoked by molecular mimicry between sialylated lipooligosaccharide (LOS) structures on the cell envelope of these bacteria and ganglioside epitopes on the human peripheral nerves, resulting in autoimmune-driven nerve destruction. Earlier, the C. jejuni sialyltransferase (Cst-II) was found to be linked to GBS and demonstrated to be involved in the biosynthesis of the ganglioside-like LOS structures. Apart from a role in pathogenicity, we report here that Cst-II-generated ganglioside-like LOS structures confer efficient bacteriophage resistance in C. jejuni. By bioinformatic analysis, it is revealed that the presence of sialyltransferases in C. jejuni and other potential GBS-related pathogens correlated significantly with the apparent degeneration of an alternative anti-virus system: type II Clusters of Regularly Interspaced Short Palindromic Repeat and associated genes (CRISPR-Cas). Molecular analysis of the C. jejuni CRISPR-Cas system confirmed the bioinformatic investigation. CRISPR degeneration and mutations in the cas genes cas2, cas1 and csn1 were found to correlate with Cst-II sialyltransferase presence (p < 0.0001). Remarkably, type II CRISPR-Cas systems are mainly found in mammalian pathogens. To study the potential involvement of this system in pathogenicity, we inactivated the type II CRISPR-Cas marker gene csn1, which effectively reduced virulence in primarily cst-II-positive C. jejuni isolates. Our findings indicate a novel link between viral defence, virulence and GBS in a pathogenic bacterium.
- Subjects :
- Gene mutation
medicine.disease_cause
natural transformation
haemophilus-influenzae
Microbiologie
Gangliosides
Campylobacter Infections
neisseria-meningitidis
pasteurella-multocida
Bacteriophages
molecular mimicry
pseudomonas-aeruginosa
biology
Bacteriologie
General Medicine
Bacteriology, Host Pathogen Interaction & Diagnostics
Molecular mimicry
Infectious Diseases
International (English)
pathogenic neisseria
Microbiology (medical)
DNA, Bacterial
ID - Infectieziekten
sialic-acid
Sialyltransferase
Virulence Factors
Virulence
Guillain-Barre Syndrome
Campylobacter jejuni
Microbiology
Bacterial genetics
SDG 3 - Good Health and Well-being
medicine
Humans
Host-Microbe Interactomics
Host Pathogen Interaction & Diagnostics
antiganglioside antibodies
Pseudomonas aeruginosa
Computational Biology
Pathogenic bacteria
Bacteriology
biology.organism_classification
bacterial infections and mycoses
Virology
lipo-oligosaccharide
Host Pathogen Interactie & Diagnostiek
Bacteriologie, Host Pathogen Interactie & Diagnostiek
biology.protein
WIAS
Subjects
Details
- Language :
- English
- ISSN :
- 09349723
- Volume :
- 32
- Issue :
- 2
- Database :
- OpenAIRE
- Journal :
- European Journal of Clinical Microbiology and Infectious Diseases
- Accession number :
- edsair.doi.dedup.....6c8ab0ffa7765337fed0f92865d6faf6