Association of<i>Helicobacter pylori</i>with Parkinson's Disease

Mridula, Kandadai Rukmini; Borgohain, Rupam; Reddy, Vupparalli Chandrasekhar; Bandaru, Venkata Chandrasekhar Srinivasarao; Turaga, Suryaprabha

doi:10.3988/jcn.2017.13.2.181

Cited by 54 publications

(43 citation statements)

References 29 publications

(41 reference statements)

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“…The mean IgG titer was significantly higher among patients with PD. Previous studies have reported lower rates of HP positivity, whereas the values obtained in our study were considerably higher (5,21). We also determined higher levels of HP antibody elevation in our control group.…”

Section: Discussionsupporting

confidence: 46%

Helicobacter pylori infection is an avoidable risk factor for Parkinson s disease

Çalık¹,

Görgün²,

Yılmaz³

et al. 2019

tjgeri

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HELICOBACTER PYLORI INFECTION IS AN AVOIDABLE RISK FACTOR FOR PARKINSON'S DISEASE Introduction: : Gram-negative bacteria such as Helicobacter pylori (HP) are becoming increasingly implicated in the etiology of Parkinson's disease (PD). This study aimed to investigate the association between PD and HP infections. Materials and Method: Eighty-three patients with PD and age-and sex-matched healthy control subjects with no history of PD were enrolled. Patients with secondary Parkinsonism and severe cognitive impairment were excluded. All patients were staged according to the Hoehn and Yahr scale. We obtained 10 mL venous blood samples from all patients and controls. The plasma was separated, and samples were stored at −200°C. IgG antibodies developing against HP were investigated using the ELISA method. Values >5 IU/ml were considered positive. Results: Eighty-three patients and 81 controls were included in the study. HP IgG was positive in 87% of the patient group and in 74% of the control group. The median antibody titer in the patient group was higher than that in the control group (p=0.0019). No significant relation was observed between disease severity and IgG positivity (p=0.947). However, a moderate correlation was observed between disease severity and mean IgG level (r=0.277, p=0.011). HP IgG positivity (OR 3.15, 95% CI 1.23-8.07, p=0.002), a family history of PD (OR 2.57, 95% CI 1.02-4.13, p= 0.03), and male gender (OR 2.05, 95% CI 0.95-6.99, p= 0.02) increase the likelihood of PD. Conclusion: HP infections may trigger various abnormal or enhanced immunological processes in patients diagnosed with PD; these abnormal immunological activities are probably involved in the disease pathogenesis.

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Section: Discussionsupporting

confidence: 46%

Helicobacter pylori infection is an avoidable risk factor for Parkinson s disease

Çalık¹,

Görgün²,

Yılmaz³

et al. 2019

tjgeri

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“…Alterations in the gut microbiome are believed to contribute to many different human health problems (Bercik et al, 2011;Boulange et al, 2016;Bravo et al, 2011;Clapp et al, 2017;Clemente et al, 2012;Dinan and Cryan, 2017b;Fung et al, 2017;Kelly et al, 2017;Ochoa-Reparaz and Kasper, 2014;Parracho et al, 2005;Tognini, 2017;Walters et al, 2014;Zhang et al, 2015). Next to the direct effects H. pylori infection on the gastrointestinal system (Camilo et al, 2017;Johnson and Ottemann, 2017;Kusters et al, 2006;Li et al, 2016;Mayer et al, 2014;Pere-Vedrenne et al, 2017;Teng et al, 2017), it has been associated with the occurrence of different neurodegenerative disorders, including Alzheimer's disease (Alvarez-Arellano and Maldonado-Bernal, 2014;Doulberis et al, 2017;Roubaud Baudron et al, 2016;Wirdefeldt et al, 2011;Wong et al, 2014) and Parkinson's disease (Alvarez-Arellano and Maldonado-Bernal, 2014;Blaecher et al, 2013;Dinan and Cryan, 2017a;Mridula et al, 2017;Mulak and Bonaz, 2015;Wirdefeldt et al, 2011;Wong et al, 2014). We recently highlighted a similar association of gastric H. suis infections in Parkinson's disease (Blaecher et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection

Gorlé

Blaecher

Bauwens

et al. 2018

Brain, Behavior, and Immunity

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Several studies suggest a link between shifts in gut microbiota and neurological disorders. Recently, we reported a high prevalence of Helicobacter suis (H. suis) in patients with Parkinson's disease. Here, we evaluated the effect of gastric H. suis infection on the brain in mice. One month of infection with H. suis resulted in increased brain inflammation, reflected in activation of microglia and cognitive decline. Additionally, we detected choroid plexus inflammation and disruption of the epithelial blood-cerebrospinal fluid (CSF) barrier upon H. suis infection, while the endothelial blood-brain barrier (BBB) remained functional. These changes were accompanied by leakage of the gastrointestinal barrier and low-grade systemic inflammation, suggesting that H. suis-evoked gastrointestinal permeability and subsequent peripheral inflammation induces changes in brain homeostasis via changes in blood-CSF barrier integrity. In conclusion, this study shows for the first time that H. suis infection induces inflammation in the brain associated with cognitive decline and that the choroid plexus is a novel player in the stomach-brain axis.

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“…In double-blind trials of biopsy-proven H. pylori eradiation [ 39 ], improved hypokinesia was independent of any (stable, long t

) anti-parkinsonian medication, and receipt of levodopa was an exclusion. Antimicrobial treatment to eliminate H. pylori infection has also been shown to improve L-dopa absorption in the gut [ 29, 30, 33, 37, 40, 41 ]. For example, Pierantozzi, et al, found that H. pylori eradicated PD patients ( n = 17) showed a significant increase in gut L-dopa absorption, in contrast with PD patients ( n = 17) given placebo, which had worsening gastritis scores and impaired L-dopa absorption [ 33 ].…”

mentioning

confidence: 99%

Stomaching the Possibility of a Pathogenic Role for Helicobacter pylori in Parkinson’s Disease

McGee

Disbrow

2018

JPD

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While a small subset of Parkinson’s disease cases have genetic causes, most cases are sporadic and may have an environmental contributor that has largely remained enigmatic. Remarkably, gastrointestinal symptoms in PD patients serve as a prodrome for the eventual motor dysfunctions. Herein, we review studies exploring a possible link between the gastric human pathogen Helicobacter pylori and PD. We provide plausible and testable hypotheses for how this organism might contribute to PD: 1) a toxin(s) produced by the bacteria; 2) disruption of the intestinal microbiome; 3) local inflammation that crosses the gut-brain axis, leading to neuroinflammation; and 4) manipulation of the pharmacokinetics of the PD drug levodopa by H. pylori, even in those not receiving exogenous levodopa. Key findings are: 1) people with PD are 1.5-3-fold more likely to be infected with H. pylori than people without PD; 2) H. pylori-infected PD patients display worse motor functions than H. pylori-negative PD patients; 3) eradication of H. pylori improves motor function in PD patients over PD patients whose H. pylori was not eradicated; and 4) eradication of H. pylori improves levodopa absorption in PD patients compared to that of PD patients whose H. pylori was not eradicated. Evidence is accumulating that H. pylori has a link with PD, but the mechanism is unclear. Future work should explore the effects of H. pylori on development of PD in defined PD animal models, focusing on the roles of H. pylori toxins, inflammation, levodopa absorption, and microbiome dysbiosis.

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Association ofHelicobacter pyloriwith Parkinson's Disease

Cited by 54 publications

References 29 publications

Helicobacter pylori infection is an avoidable risk factor for Parkinson s disease

Helicobacter pylori infection is an avoidable risk factor for Parkinson s disease

The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection

Stomaching the Possibility of a Pathogenic Role for Helicobacter pylori in Parkinson’s Disease

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