摘要
Helicobacter pylori （H. pylori） virulence factors pro- mote the release of various chemoattractants/inflam- matory mediators, including mainly the neutrophil- attractant chemokine interleukin-8 and neutrophil- activating protein （NAP）, involved in H. pylor/-induced gastric pathologies. Co-administration of Chios mastic gum （CMG）, which inhibits H. pylor/NAP, with an H. pylori eradication regimen might add clinical benefits against H. pylori-related gastric pathologies, but pos- sibly 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 gener- ating and maintaining the H. pylori-associated gastric inflammatory response and H. pylor/NAP is a promising vaccine candidate against H. pylori infection （H. pylori-1）, concerns regarding its potential drawbacks, particularly neurogenic ones, due to possible cross- mimicry, should be considered. Possible cross-mimicry between H. p, vlor/ 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 im- plicated in inducing blood-brain barrier （BBB） disrup- tion, including inflammatory mediators （e.g., cytokines and chemokines induced by H. pylor/-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 sclero- sis pathogenesis. Relative studies show a strong asso- ciation between H. pylori-I and MS. H. pylor/-I induces humoral and cellular immune responses that, owing to the sharing of homologous epitopes （molecular mim- icry）, cross-react wit
Helicobacter pylori (H.pylori) virulence factors promote the release of various chemoattractants/inflammatory mediators,including mainly the neutrophilattractant chemokine interleukin-8 and neutrophilactivating 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 crossmimicry,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
