title: Potential implications of Helicobacter pylori-related neutrophil-activating protein.
abstract: Helicobacter pylori (H. pylori) virulence factors promote the release of various chemoattractants/inflammatory mediators, including mainly the neutrophil-attractant chemokine interleukin-8 and neutrophil-activating protein (NAP), involved in H. pylori-induced gastric pathologies. Co-administration of Chios mastic gum (CMG), which inhibits H. pylori NAP, with an H. pylori eradication regimen might add clinical benefits against H. pylori-related gastric pathologies, but possibly not CMG as main therapy. Although H. pylori NAP and other H. pylori-related cytotoxins [i.e., vaculating cytotoxin (VacA)] appear to play a major role in generating and maintaining the H. pylori-associated gastric inflammatory response and H. pylori NAP is a promising vaccine candidate against H. pylori infection (H. pylori-I), concerns regarding its potential drawbacks, particularly neurogenic ones, due to possible cross-mimicry, should be considered. Possible cross-mimicry between H. pylori NAP and/or bacterial aquaporin (AQP) and neural tissues may be associated with the anti-AQP-4 antibody-related neural damage in multiple sclerosis (MS)/neuromyelitis optica patients. Moreover, the sequence homology found between H. pylori VacA and human Na+/K+-ATPase A subunit suggests that antibodies to VacA involve ion channels in abaxonal Schwann cell plasmalemma resulting in demyelination in some patients. A series of factors have been implicated in inducing blood-brain barrier (BBB) disruption, including inflammatory mediators (e.g., cytokines and chemokines induced by H. pylori-I) and oxidative stress. BBB disruption permits access of AQP4-specific antibodies and T lymphocytes to the central nervous system, thereby playing a major role in multiple sclerosis pathogenesis. Relative studies show a strong association between H. pylori-I and MS. H. pylori-I induces humoral and cellular immune responses that, owing to the sharing of homologous epitopes (molecular mimicry), cross-react with components of nerves, thereby contributing and perpetuating neural tissue damage. Finally, H. pylori NAP also plays a possible pathogenetic role in both gastric and colon oncogenesis.
authors.forename: Jannis
authors.initials: J
authors.lastname: Kountouras
authors.forename: Christos
authors.initials: C
authors.lastname: Zavos
authors.forename: Georgia
authors.initials: G
authors.lastname: Deretzi
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Gavalas
authors.forename: Dimitrios
authors.initials: D
authors.lastname: Chatzopoulos
authors.forename: Panagiotis
authors.initials: P
authors.lastname: Katsinelos
authors.forename: Elena
authors.initials: E
authors.lastname: Tsiaousi
authors.forename: Stergios
authors.initials: S
authors.lastname: Gagalis
authors.forename: Stergios A
authors.initials: SA
authors.lastname: Polyzos
authors.forename: Ioannis
authors.initials: I
authors.lastname: Venizelos
mesh_terms: D000900:Anti-Bacterial Agents / Q000627:therapeutic use*; D001426:Bacterial Proteins / Q000378:metabolism*; D016481:Helicobacter Infections / Q000188:drug therapy*; D016480:Helicobacter pylori / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D012116:Resins, Plant / Q000627:therapeutic use*
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D012116:Resins, Plant