ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2013
A novel link between Campylobacter jejuni bacteriophage defence, virulence and Guillain-Barré syndrome.
Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 1 of them a synthesis that pooled it.
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Who cites it
90 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
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- CRISPR-Cas systems target endogenous genes to impact bacterial physiology and alter mammalian immune responses.Molecular biomedicine · 2022Review
- Mucin induces CRISPR-Cas defense in an opportunistic pathogen.Nature communications · 2022Article
- Alternative functions of CRISPR-Cas systems in the evolutionary arms race.Nature reviews. Microbiology · 2022Review
- Th1/Th17-mediated Immunity and Protection from Peripheral Neuropathy in Wildtype and IL10Comparative medicine · 2022Article
- Identification of RNA Binding Partners of CRISPR-Cas Proteins in Prokaryotes Using RIP-Seq.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Engineered CRISPR-Cas systems for the detection and control of antibiotic-resistant infections.Journal of nanobiotechnology · 2021Review
- crRNA complementarity shifts endogenous CRISPR-Cas systems between transcriptional repression and DNA defense.RNA biology · 2021Article
- Detection of Campylobacter jejuni diversity by clustered regularly interspaced short palindromic repeats (CRISPR) from an animal farm.Veterinary medicine and science · 2021Article
- AMicrobial genomics · 2021Article
30 more citing papers are in PubMed but not listed here.
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18 authors at 8 institutions in 3 countries.
Funding
Abstract
Guillain-Barré 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.
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