Impaired cytokine production by peripheral blood mononuclear cells and monocytes/macrophages in Parkinson's disease
Abstract:Objective: Although the pathogenesis of Parkinson's disease (PD) is still unknown, several reports suggest the presence of immunological abnormalities in the patients with PD such as impaired T cell responses or cytokine production by the peripheral immune system. Material and methods: In this study, we examined cytokine production by peripheral blood mononuclear cells (PBMC) and monocyte/macrophages (PBM) in the patients with idiopathic PD, using age‐related healthy donors as a normal control and cerebrovascular diseases (CVD) as a disease control. Results: Production of TNF‐α, IL‐1α, IL‐1β and IL‐6 by PBMC and TNFα by PBM were significantly lower in the patients with PD as compared to the control groups. IFN‐γ production by LPS‐stimulated PBMC in the patients with PD was also significantly lower than that in control groups. Cytokine production by PBMC from the patients with CVD who had a similar disability as the patient group was not significantly different from those in normal controls. Thus, impaired production of inflammatory cytokines may not be due to the mental and physical stress caused by their disability. Conclusion: In the patients with PD, a significant negative correlation was noted in IL‐1α, IL‐1β and IL‐6 levels produced by LPS‐stimulated PBMC and Hoehn–Yahr disability score of the patients, suggesting that the impaired cytokine production may progress with disease progression. These abnormalities in cytokine production may not be primary but may affect the prognosis of PD.
Document Type: Original Article
Affiliations: 1: Department of Neurology, Nagoya City Koseiin Geriatric Hospital, Nagoya 465‐8610, japan, 2: Joint Research Division for Therapies against Intractable Diseases, Institute for Comprehensive Medical Science, Fujita Health University, Toyoake Aichi 470‐1192, Japan, 3: Department of Neurology, Nara Medical University, 840 Shijo‐cho, Kashihara 634, Japan
Publication date: 2000-03-01