RESUMO
Objective To investigate the pathogenic mechanism of Campylobacter jejuni(C.jejuni) associated with Guillain-Barré syndrome(GBS) and provide strategy for gene modification, the cstⅡ gene from 8 GBS-associated C.jejuni strains were compared with that from 3 GBS-unrelated C.jejuni strains, getting the base and amino acid mutations, the changes of secondary structures and finding the region which may be responsible for the pathogenicity of C.jejuni inducing GBS. Methods Three GBS-associated C.jejuni strains isolated from stools of GBS patients in north China were selected and cultured, which has been confirmed as GBS-associated by animal model. After sequencing the genome of them, the nucleotide sequences of cstⅡ gene were got through sequence alignment. The nucleotide sequences and deduced amini acid sequences of 3 GBS-associated cstⅡ genes were compared with that from 3 GBS-unrelated C.jejuni strains through bioinformatics software, getting the base and amino acid mutations, the changes of secondary structures. Other 5 GBS-associated cstⅡ genes were also aligned to know whether the differences we got above makes sense. In this way the genetic differences between two kinds of C.jejuni strains may be found and speculating the gene region related to the pathogenicity of GBS became possible. Results The cstⅡgene of 3 GBS-associated C.jejuni strains were all composed of 876 base pairs. Compared with GBS-unrelated C.jejuni strains, there were 9 consistent mutation sites in cstⅡ gene of LL and QYT stains, leading to 3 consistent amino acid mutation. The amino acid mutation of 114 and 182 sites in LL and QYT stains existed in other 5 GBS-associated C.jejuni strains. The sole amino acid mutation of ZHX strain -169 site, located near the 182 site. The seventh α-helix(165-180 region)of the secondary structure of the amino acid sequence from GBS-associated strains were shorter than that from GBS-unrelated strains, and the shorter regions were opened to form β-sheet or coli, which also existed in other GBS-related strains in this study.75% of the GBS-associated cstⅡ genes were Asn-51, while 25% of the GBS-associated and all of the GBS-unrelated cstⅡ genes were Thr-51.LL strain showed highly identity to other GBS-unrelated strains in this study. Conclusion The 165-180 segment of secondary structures in cstⅡ gene from local 3 GBS-associated C.jejuni strains are probably the responsible region involved in inducing GBS. The senior structure changes in this region may affect the activity of sialyltransferase and the structures of ganglioside epitope, so that the C.jejuni can acquire the pathogenicity of GBS. This finding may give a clue to genetic modified site. The bi-functional cstⅡ of C.jejuni may be related to the pathogenicity of GBS. The cstⅡ of LL strain to some extent represents the characteristics of Asian strains, which may directs strains monitoring.