H. pylori and Parkinson’s disease: Meta-analyses including clinical severity

Dardiotis, Efthimios; Tsouris, Zisis; Mentis, Alexios‐Fotios A.; Siokas, Vasileios; Michalopoulou, Amalia; Sokratous, Maria; Dastamani, Metaxia; Bogdanos, Dimitrios P.; Deretzi, Georgia; Kountouras, Jannis

doi:10.1016/j.clineuro.2018.09.039

Cited by 81 publications

(59 citation statements)

References 58 publications

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“…Subgroup analysis revealed a higher OR in Asia than in Europe (1.99 and 1.55, respectively) (22). In another meta-analysis, HP infection was identified as a risk factor in terms of PD, and a decrease in UPDRS scores, indicating severity of PD, was achieved with HP eradication (23). In our study, when all potential confounding factors were added together, HP increased the risk of PD 3.15fold.…”

Section: Discussionsupporting

confidence: 45%

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: 45%

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

Çalık¹,

Görgün²,

Yılmaz³

et al. 2019

tjgeri

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“…In association with dysbiosis in one PD cohort (Hill‐Burns et al., ), our group has been able to detect increased levels of NFkB‐regulated inflammatory factors in the stool of patients with sporadic PD relative to household controls (Houser et al., ), raising the possibility that gut inflammation may create a permissive environment for non‐motor gastrointestinal symptoms and perhaps exacerbation of motor symptoms. For instance, a recent meta‐analysis suggests that prevalence of infections with Helicobacter pylori is higher among PD patients; and that those PD patients infected with H. pylori showed more severe motor symptoms, suggesting that the infections can aggravate the disease (Dardiotis et al., ). For further consideration of these hypotheses, we refer the reader to a review on how intestinal inflammation could potentially contribute to a‐syn upregulation and aggregation in peripheral organs such as the gut that are connected anatomically to the gut in various ways and therefore potentially involved in any propagation of a‐syn from the periphery to the CNS (Houser & Tansey, ).…”

Section: Infections As Putative Players In the Risk Of Developing Parmentioning

confidence: 99%

Immune system responses in Parkinson's disease: Early and dynamic

Tansey

Romero‐Ramos

2018

Eur J of Neuroscience

112

115

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The neuropathological hallmarks of Parkinson's disease (PD) are the degeneration and death of dopamine‐producing neurons in the ventral midbrain, the widespread intraneuronal aggregation of alpha‐synuclein (α) in Lewy bodies and neurites, neuroinflammation, and gliosis. Signs of microglia activation in the PD brain postmortem as well as during disease development revealed by neuroimaging, implicate immune responses in the pathophysiology of the disease. Intensive research during the last two decades has advanced our understanding of the role of these responses in the disease process, yet many questions remain unanswered. A transformative finding in the field has been the confirmation that in vivo microglia are able to respond directly to pathological a‐syn aggregates but also to neuronal dysfunction due to intraneuronal a‐syn toxicity well in advance of neuronal death. In addition, clinical research and disease models have revealed the involvement of both the innate and adaptive immune systems. Indeed, the data suggest that PD leads not only to a microglia response, but also to a cellular and humoral peripheral immune response. Together, these findings compel us to consider a more holistic view of the immunological processes associated with the disease. Central and peripheral immune responses aimed at maintaining neuronal health will ultimately have consequences on neuronal survival. We will review here the most significant findings that have contributed to the current understanding of the immune response in PD, which is proposed to occur early, involve peripheral and brain immune cells, evolve as neuronal dysfunction progresses, and is likely to influence disease progression.

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“…Additionally, not all detection methods can identify long‐lasting antibodies; for instance, immunoblot can detect antibodies against CagA, which may present even for more than a decade post‐eradication, contrary to those identified by ELISA which do not last so long . Furthermore, in order for the studies to be more concordant, we excluded results from methods such as histological examination, which is however more reliable concerning H pylori infection …”

Section: Discussionmentioning

confidence: 99%

“…Both the localized and the systemic immune responses, involving innate and adaptive immunity, can be induced by H pylori . Systemic immune and inflammatory responses to H pylori have also been described; for example, relevant studies have hinted towards a potential connection between H pylori infection and the pathogenic procedures of a plethora of systemic and organ‐specific immunological/autoimmune disorders, including those with neurodegenerative manifestation . In this regard, a considerable amount of reports has linked this pathogen to the development of peripheral neuropathies, such as Guillain‐Barré syndrome (GBS) and Miller Fisher syndrome (MFS) …”

Section: Introductionmentioning

confidence: 99%

Association between Helicobacter pylori infection and Guillain‐Barré Syndrome: A meta‐analysis

Dardiotis

Sokratous

Tsouris

et al. 2020

Eur J Clin Investigation

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Background: Helicobacter pylori (H pylori) is a Gram-negative bacterium, considered to trigger autoimmune gastrointestinal disorders. This pathogen has also been linked to the autoimmune sequelae in extra-gastrointestinal diseases and peripheral neuropathies. Guillain-Barré syndrome (GBS) is a serious autoimmune demyelinating disorder of peripheral nerves, usually with a post-infectious onset. About 30% of cases of GBS attributed to by Campylobacter jejuni, so, H pylori, could be also involved. Growing evidence suggests the likely involvement of H pylori infection in the development of GBS. The aim of the current study was to therefore estimate the prevalence of H pylori antibodies in GBS. Methods: A search of the literature was performed, using the PUBMED database, until December 2018. Data were extracted from six case-control studies, and a stratification analysis was conducted according to cerebrospinal fluid (CSF) or serum detection material. Results: Among 29 records found, 6 studies met in the inclusion criteria for the metaanalysis. In the CSF subgroup, 105 participants were involved (40 GBS patients and 65 controls), while the serum subgroup included 325 participants (152 GBS and 173 controls). Data were combined using a fixed-effects model. Anti-H pylori IgG were significantly more prevalent in GBS patients compared to controls, in both CSF (95% CI: 9. OR: 42.45, Pz < .00001) and serum (95% CI: 1.30-4.11, OR: 2.31, Pz: .004) subgroups. Conclusion: The present meta-analysis showed a strong association between GBS and the presence of H pylori antibodies, especially in CSF, thereby suggesting a role of H pylori infection in the pathophysiology of GBS. K E Y W O R D Santi-H pylori IgG, antibodies, Guillain-Barré Syndrome, Helicobacter pylori, seropositivity

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H. pylori and Parkinson’s disease: Meta-analyses including clinical severity

Cited by 81 publications

References 58 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

Immune system responses in Parkinson's disease: Early and dynamic

Association between Helicobacter pylori infection and Guillain‐Barré Syndrome: A meta‐analysis

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