Assuntos
Infecções por Helicobacter/imunologia , Helicobacter pylori/imunologia , Encefalopatia Hepática/imunologia , Hipertensão Portal/imunologia , Feminino , Infecções por Helicobacter/complicações , Infecções por Helicobacter/patologia , Infecções por Helicobacter/terapia , Encefalopatia Hepática/etiologia , Encefalopatia Hepática/patologia , Encefalopatia Hepática/terapia , Humanos , Hipertensão Portal/complicações , Hipertensão Portal/patologia , Hipertensão Portal/terapia , MasculinoAssuntos
Transformação Celular Neoplásica/patologia , Colo/microbiologia , Infecções por Helicobacter/fisiopatologia , Helicobacter pylori/patogenicidade , Adenoma/metabolismo , Adenoma/microbiologia , Estudos de Casos e Controles , Transformação Celular Neoplásica/metabolismo , Colo/metabolismo , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/microbiologia , Humanos , Receptores de Hialuronatos/metabolismoAssuntos
Glaucoma/prevenção & controle , Infecções por Helicobacter/tratamento farmacológico , Helicobacter pylori , Doenças do Nervo Óptico/prevenção & controle , Animais , Antibacterianos/uso terapêutico , Apoptose , Sobrevivência Celular , Glaucoma/microbiologia , Humanos , Doenças do Nervo Óptico/microbiologia , Células Ganglionares da Retina/efeitos dos fármacos , Células Ganglionares da Retina/microbiologiaRESUMO
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.