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Taxonomic group: bacteria / Proteobacteria (Phylum: Proteobacteria)
Associated disease: infection due to Campylobacter jejuni [ICD11: XN4Q5

]

NCBI PubMed ID: 20593269
Publication DOI: 10.1007/978-90-481-9078-2_10
Publisher: Springer Science+Business Media B.V.
Editors: Wang X, Quinn PJ
Correspondence: anthony.moran

nuigalway.ie
Institutions: Laboratory of Molecular Biochemistry, Microbiology, School of Natural Sciences, National University of Ireland, Galway, Ireland

Both Helicobacter pylori and Campylobacter jejuni are highly prevalent Gram-negative microaerophilic bacteria which are gastrointestinal pathogens of humans; H. pylori colonizes the gastroduodenal compartment and C. jejuni the intestinal mucosa. Although H. pylori causes chronic gastric infection leading to gastritis, peptic ulcers and eventually gastric cancer while C. jejuni causes acute infection inducing diarrhoeal disease, the endotoxin molecules of both bacterial species contrastingly contribute to their pathogenesis and the autoimmune sequelae each induces. Compared with enterobacterial endotoxin, that of H. pylori has significantly lower endotoxic and immuno-activities, the molecular basis for which is the underphosphorylation and underacylation of the lipid A component that interacts with immune receptors. This induction of low immunological responsiveness by endotoxin may aid the prolongation of H. pylori infection and therefore infection chronicity. On the other hand, this contrasts with acute infection-causing C. jejuni where overt inflammation contributes to pathology and diarrhoea production, and whose endotoxin is immunologically and endotoxically active. Futhermore, both H. pylori and C. jejuni exhibit molecular mimicry in the saccharide components of their endotoxins which can induce autoreactive antibodies; H. pylori expresses mimicry of Lewis and some ABO blood group antigens, C. jejuni mimicry of gangliosides. The former has been implicated in influencing the development of inflammation and gastric atrophy (a precursor of gastic cancer), the latter is central to the development of the neurological disorder Guillain-Barre syndrome. Both diseases raise important questions concerning infection-induced autoimmunity awaiting to be addressed.

lipid A, Campylobacter jejuni, molecular mimicry, Helicobacter pylori, bacterial pathogenesis

Structure type: oligomer
Location inside paper: p.226, fig.10.5,H
Trivial name: oligosaccharide GD1b and GD2 mimics
Contained glycoepitopes: IEDB_120354,IEDB_123890,IEDB_130648,IEDB_130650,IEDB_130676,IEDB_130678,IEDB_130679,IEDB_130681,IEDB_130683,IEDB_130684,IEDB_130685,IEDB_134627,IEDB_136044,IEDB_136794,IEDB_137472,IEDB_137473,IEDB_140087,IEDB_140088,IEDB_140090,IEDB_141794,IEDB_142487,IEDB_142488,IEDB_146100,IEDB_146664,IEDB_147450,IEDB_147451,IEDB_149174,IEDB_150933,IEDB_150937,IEDB_153198,IEDB_153199,IEDB_153777,IEDB_153778,IEDB_1625329,IEDB_190606,IEDB_2189047,IEDB_433718,IEDB_547903,IEDB_858580,IEDB_983931,SB_116,SB_144,SB_164,SB_165,SB_166,SB_170,SB_171,SB_172,SB_187,SB_192,SB_195,SB_23,SB_24,SB_25,SB_35,SB_37,SB_39,SB_42,SB_6,SB_68,SB_7,SB_76,SB_8,SB_84,SB_88,SB_96

Biological activity: GD1b and GD2 mimics

Related record ID(s): 25352, 25763, 25764, 25765, 25766, 25767, 25768, 25769, 25770, 25771, 25772, 25773, 25774, 25775, 25776, 25777, 25778, 31114, 31115, 31116
NCBI Taxonomy refs (TaxIDs): 354242
Reference(s) to other database(s): GTC:G59052OX
Show glycosyltransferases

There is only one chemically distinct structure:

CC(=O)N[C@@H]1[C@@H](O)C[C@](O[C@H]2[C@@H](O[C@@H]3O[C@H](CO)[C@H](O)[C@H](O[C@@H]4O[C@H](CO)[C@H](O)[C@H](O)[C@H]4O)[C@H]3NC(C)=O)[C@@H](CO)O[C@@H](O[C@@H]3[C@@H](CO)O[C@@H](O[C@H]4[C@@H](O)[C@H](O)[C@@H]([C@@H](O)CO)O[C@@H]4O[C@@H]4[C@H](O)[C@@H](O[C@@H]5[C@H](O)C[C@](O)(C(=O)O)O[C@@H]5[C@H](O)CO)O[C@H]([C@H](CO)OP(=O)(O)OCCN)[C@H]4O[C@@H]4O[C@H](CO)[C@@H](O)[C@H](O)[C@H]4O)[C@H](O)[C@H]3O)[C@@H]2O)(C(=O)O)O[C@H]1[C@H](O)[C@@H](CO)O[C@]1(C(=O)O)C[C@H](O)[C@@H](NC(C)=O)[C@H]([C@H](O)[C@H](O)CO)O1

SVG MW SMILES 3D mol Ionize