An antibody to VacA of Helicobacter pylori in cerebrospinal fluid from patients with Guillain-Barre syndrome

Increased levels of Helicobacter pylori IgG antibodies in aqueous humor of patients with primary open-angle and exfoliation glaucoma

“…C. jejuni, a principal cause of gastroenteritis, is the most common antecedent infection in Guillain-Barre syndrome, an inflammatory neuropathy. In addition, 46% of patients with Guillain-Barre syndrome have specific IgG antibodies to VacA of H. pylori in the cerebrospinal fluid, and the sequence homology found between 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 within the cerebrospinal fluid [4].…”

“…For this purpose, blood 885 some glaucoma patients [3,27,31,33]. The concept that the immune system may facilitate the progression of glaucomatous optic neuropathy has gained more credence recently with evidence accumulating for the causative role of autoantibodies in a number of peripheral neuropathies, e.g., Guillain-Barre, and is mainly, but not exclusively, associated with normal-tension glaucoma patients [4].…”

Eradication of Helicobacter pylori may be beneficial in the management of Alzheimer’s disease

“…In addition, 46% of patients with GBS have specific IgG antibodies to VacA of Hp in the cerebrospinal fluid, which are probably associated with some components of the peripheral nerve myelin, thereby showing considerable demyelination of the peripheral nerves; the sequence homology found between 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 these patients [5,27]. In this regard, it is relevant to speculate that such anti-Hp-mediated apoptotic mechanisms might also lead to degeneration of ganglion cells, thereby contributing to AD neuropathy or other degenerative neuropathies, such as glaucoma, defined as ocular AD.…”

“…(4) Stimulating mononuclear cells to produce a tissue factor-like procoagulant that converts fibrinogen into fibrin [25]. (5) Causing the development of cross mimicry between endothelial and Hp antigens. (6) Producing reactive oxygen metabolites (ROMs) and circulating lipid peroxides [24,25], which have been implicated in the pathophysiology of AD [31,45]; accumulating evidence suggests that ROMs are potent deleterious agents causing cell death or other forms of irreversible cell damage, and oxidative stress participates in the neuronal loss in AD [25,48].…”

Helicobacter pylori IgG Antibodies in Aqueous Humor and Serum of Subjects With Primary Open Angle and Pseudo-exfoliation Glaucoma in a South Indian Population

“…[6][7][8] The concept of immune system facilitating the development of glaucomatous optic neuropathy in some susceptible individuals has gained more credence with evidence accumulating for the causative role of autoantibodies in a number of peripheral neuropathies, for example, Guillain-Barre syndrome. 9 The possibility of an infectious pathogenetic mechanism in PXFG was suggested in one Norwegian study, where the prevalence of PXFG was significantly more common in spouses of patients with the disease. 10 Kountouras et al 11 have established a higher prevalence of H. pylori infection in the sera of patients with POAG and PXFG compared with age-matched control participants with anemia, in a Greek population.…”