Expression of inflammatory cytokines in CADASIL and their associations with clinical and neuroimaging features
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Published on: June 13, 2011
Li Bai1,2,3,4, Haotian Yan1,2,3, Zhongao Wang1,2,3
1Department of Neurology, Peking University First Hospital, Beijing, China.
Insights
Inflammatory cytokines are elevated in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) patients. Increased tumor necrosis factor-beta (TNF-β) correlates with disease severity, suggesting its role in CADASIL progression.
Area of Science:
- Neuroimmunology
- Vascular Neurology
Background:
- Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic small vessel disease.
- Inflammation is implicated in the pathogenesis of cerebrovascular diseases.
Purpose of the Study:
- To investigate the expression levels of various inflammatory cytokines in CADASIL patients.
- To determine the association between these cytokine levels and clinical/MRI features.
Main Methods:
- Recruited 54 CADASIL patients and 28 healthy controls.
- Measured peripheral blood levels of 12 inflammatory cytokines (IFN-γ, TNF-α, TNF-β, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-17F, IL-22).
- Analyzed correlations with clinical (mRS, MMSE, apathy) and MRI (CMBs) data.
Main Results:
- Most inflammatory cytokines were significantly higher in CADASIL patients compared to controls.
- Elevated TNF-β levels correlated with higher modified Rankin Scale (mRS) scores, lower Mini-Mental State Examination (MMSE) scores, increased apathy, and a greater number of cerebral microbleeds (CMBs).
Conclusions:
- CADASIL is characterized by a diffuse inflammatory response.
- TNF-β upregulation is linked to increased CMB burden and poorer clinical outcomes in CADASIL.
- The TNF-related inflammatory pathway may contribute to CADASIL pathogenesis and progression.
Objectives:
The aim of our study is to explore the expression levels of inflammatory cytokines in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), and to assess the correlation between inflammatory cytokines and clinical/magnetic resonance imaging (MRI) features of the patients.
Methods:
We recruited 54 patients with CADASIL and 28 healthy controls and detected the expression levels of the following inflammatory cytokines in peripheral blood: interferon (IFN)-γ, tumor necrosis factor (TNF)-α, TNF-β, interleukin (IL)-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-17F, and IL-22. We also analyzed the relationship between the expression levels of the inflammatory cytokines and the clinical/MRI features.
Results:
The expression of most inflammatory cytokines were significantly higher in CADASIL patients than in healthy controls, including IFN-γ (z = -5.335, P < 0.001), TNF-α (z = -4.880, P < 0.001), TNF-β (z = -2.401, P = 0.019), IL-1β (z = -2.831, P = 0.007), IL-4 (z = -4.039, P < 0.001), IL-5 (z = -4.523, P < 0.001), IL-6 (z = -3.545, P < 0.001), IL-8 (z = -5.667, P < 0.001), IL-17F (z = -3.986, P < 0.001) and IL-22 (z = -5.325, P < 0.001). The increased expression level of TNF-β was correlated with abnormal mRS scores in patients with CADASIL (odds ratio [OR] = 6.147, 95% CI: 1.324-28.535; P = 0.020) after adjustment for age, sex, history of hypertension and history of diabetes. The expression level of TNF-β was also associated with MMSE (β = -0.281, 95% CI:-5.325-0.866, P = 0.008) and apathy scores (β = 0.388, 95% CI:2.554-16.328, P = 0.008) after adjusting for age, sex, educational years, history of hypertension and history of diabetes. There was also a positive correlation between the expression level of TNF-β and the number of CMBs in deep (β = 0.314, 95% CI:2.989-39.461, P = 0.023) and lobar region (β = 0.433, 95% CI:15.363-59.857, P = 0.001) after adjusting for age, sex, history of hypertension and history of diabetes.
Conclusions:
Our results indicate that diffuse inflammatory pathway activation occurs in CADASIL. The increased expression level of TNF-β was associated with higher CMBs burden and poor clinical scores. Our findings suggest that the inflammatory pathway, particularly the TNF-related inflammatory pathway, may be involved in the disease progression of CADASIL.
