Evaluation of seropositivity developed against specific antigens of helicobacter pylori in neurodegenerative diseases

Introduction: It is suggested that Helicobacter pylori (Hp) can reach the brain via the oral-nasal-olfactory route, through Hp-infected monocytes in the disrupted blood-brain barrier (BBB), or through a rapid retrograde neural network leading to neurodegeneration from the gastrointestinal tract (GIS) and may lead to neurodegenerative diseases such as Alzheimer’s (AD), Parkinson’s (PD) and Multiple sclerosis (MS). In this study, we aimed to evaluate the possible immunopathogenesis relationship between Hp-specific antigens and neurodegenerative diseases by determining the frequency of seropositivity against different specific antigens of Hp in diseases such as AD, PD and MS. Methods: In our cross-sectional, retrospective case-control study, the immunoreactivity frequencies of Hp-specific and non-specific CagA (p120), VacA (p95), p75, FSH (p67), UreB (p66), HSP homolog (p57), flagellin (p54), p50, p41, p33, OMP (p30), UreA (p29), p26, OMP (p19), p17 antigens were determined by Western Blot method in 36 AD, 35 PD, 91 MS cases with Hp-IgG reactivity, and 55 controls without a neurodegenerative/demyelinating by ELISA method. Results: No significant difference was found between the immunoreactivity frequencies of Hp antigens between AD and control groups (p>0.05). In the multivariate logistic analysis performed for PD cases, age ≥ 50 and immunoreactivity frequency of p19 were found to be independent risk factors (OR: 36.752, p<0.05) (OR: 5.570, p<0.05). In MS cases, immunoreactivity frequency of p17 antigen was found to be a risk factor (OR: 2.646, p<0.05). In addition, the mean level of Hp-IgG reactivity was found to be negatively associated with MS development (indicating an inverse correlation) in the control group compared to the MS group (OR: 0.585, p < 0.05). Furthermore, logistic regression analysis in the total study group revealed that the immunoreactivity frequency of the p17 antigen was identified as a risk factor for MS (OR: 2.438, p<0.05). Conclusion: Our data on AD cases are insufficient. In PD cases, the significantly higher frequency of immunoreactivity to the Hp-p19 antigen in individuals aged ≥50 years (OR=5.570) is noteworthy. In the MS group, the significantly high detection of Hp p17 antigen and its presence as a risk factor (OR=2.646), and the significantly high detection of p26 antigen suggest the relationship between these antigens and the MS development process. However, it is a fact that new and many prospective cohort-based case-control studies are needed to reveal this more clearly.