| Literature DB >> 32110976 |
Pedro Guirado1, Sonia Paytubi1, Elisenda Miró2, Yaidelis Iglesias-Torrens2,3, Ferran Navarro2,3, Marta Cerdà-Cuéllar4, Camille Stephan-Otto Attolini5, Carlos Balsalobre1, Cristina Madrid1.
Abstract
Campylobacter jejuni causes campylobacteriosis, a bacterial gastroenteritis with high incidence worldwide. Moreover, C. jejuni infection can trigger the polyneuropathic disorder denominated Guillain-Barré syndrome (GBS). The C. jejuni strains that can elicit GBS carry either wlaN or cgtB, coding both genes for a β-1,3-galactosyltransferase enzyme that is required for the production of sialylated lipooligosaccharide (LOSSIAL). We described a differential prevalence of the genes wlaN and cgtB in C. jejuni isolates from three different ecological niches: humans, broiler chickens, and wild birds. The distribution of both genes, which is similar between broiler chicken and human isolates and distinct when compared to the wild bird isolates, suggests a host-dependent distribution. Moreover, the prevalence of the wlaN and cgtB genes seems to be restricted to some clonal complexes. Gene sequencing identified the presence of new variants of the G- homopolymeric tract within the wlaN gene. Furthermore, we detected two variants of a G rich region within the cgtB gene, suggesting that, similarly to wlaN, the G-tract in the cgtB gene mediates the phase variation control of cgtB expression. Caco-2 cell invasion assays indicate that there is no evident correlation between the production of LOSSIAL and the ability to invade eukaryotic cells.Entities:
Keywords: Campylobacter; Guillain-Barré syndrome; cgtB; lipooligosaccharide; wlaN
Year: 2020 PMID: 32110976 DOI: 10.3390/microorganisms8030325
Source DB: PubMed Journal: Microorganisms ISSN: 2076-2607