Potential implications of Helicobacter pylori-related neutrophil-activating protein.
Title | Potential implications of Helicobacter pylori-related neutrophil-activating protein. |
Publication Type | Journal Article |
Year of Publication | 2012 |
Authors | Kountouras, J., Zavos C., Deretzi G., Gavalas E., Chatzopoulos D., Katsinelos P., Tsiaousi E., Gagalis S., Polyzos S. A., & Venizelos I. |
Journal | World J Gastroenterol |
Volume | 18 |
Issue | 5 |
Pagination | 489-90 |
Date Published | 2012 Feb 07 |
ISSN | 2219-2840 |
Keywords | Anti-Bacterial Agents, Bacterial Proteins, Helicobacter Infections, Helicobacter pylori, Humans, Inflammation, Resins, Plant |
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. |
DOI | 10.3748/wjg.v18.i5.489 |
Alternate Journal | World J. Gastroenterol. |
PubMed ID | 22346256 |
PubMed Central ID | PMC3270508 |