Change of intestinal microbiota in cerebral ischemic stroke patients.

BACKGROUND: Gut microbiota has been suggested to play a role in stroke patients. Nevertheless, little is known about gut microbiota and the clinical indexes in stroke patients. METHODS: Total of 30 cerebral ischemic stroke (CI) patients and 30 healthy control were enrolled in this study and the fecal gut microbiota was profiled via Illumina sequencing of the 16S rRNA V1-V2. The National Institutes of Health Stroke Scale (NIHSS) were used to quantify stroke severity and modified Rankin scale (mRS) to assess outcome for CI patients. The correlations between the clinical indexes and microbiota were evaluated. RESULTS: Though the microbial α-diversity and structure is similar between CI patients and healthy controls, the gut microbiota of CI patients had more short chain fatty acids producer including Odoribacter, Akkermansia, Ruminococcaceae_UCG_005 and Victivallis. We also found that the special microbes were correlation with serum index, such as norank_O_ _Mollicutes_RF9, Enterobacter, Ruminococcaceae_UCG-002 were negative correlation with LDL (r = - 0.401, P < 0.01), HDL (r = - 0.425, P < 0.01) and blood glucose (r = - 0.439, P < 0.001), while the HDL was significantly positive correlation with the genus Ruminococcus_1 (r = 0.443, P < 0.001). The Christensenellaceae_R-7_group and norank_f_Ruminococcaceae was significantly positive correlation with NIHSS1M (r = 0.514, P < 0.05; r = 0.449, P < 0.05) and mRS (r = 0.471, P < 0.05, r = 0.503, P < 0.01), respectively. On the other hand, the genus Enterobacter was significantly negative correlation with NIHSS1M (r = 0.449, P < 0.05) and mRS (r = 0.503, P < 0.01). CONCLUSIONS: This study suggests that CI patients showed significant dysbiosis of the gut microbiota with enriched short chain fatty acids producer, including Odoribacter, Akkermansia. This dysbiosis was correlation with the outcomes and deserves further study.

Abnormal subpopulations of peripheral blood lymphocytes are involved in Parkinson's disease.

BACKGROUND: Abnormal immune responses are involved in the development of Parkinson's disease (PD), and also affect peripheral blood lymphocytes. The profile of lymphocyte subsets in peripheral blood and whether it is relevant to the clinical features of PD patients remains controversial. METHODS: To explore the role of peripheral blood lymphocytes (NK cells, B cells, CD3+ T cells, CD3+CD4+ T cells and CD3+CD8+ T cells) in the development of PD, a case-control study including 127 patients and 148 healthy controls was conducted, and peripheral blood lymphocyte subpopulations of participants were analysed by a FACSCalibur flow cytometer. RESULTS: PD patients had a significantly higher percentage of NK cells and a lower percentage of CD3+ T cells and CD3+CD4+ T cells than controls [16.4% (12.3%) vs. 12.6% (6.2%), 63.7% (14.2%) vs. 69.0% (6.6%), 33.1% (13.1%) vs. 38.9% (7.6%), P<0.05, respectively]. Through a binary logistic regression model adjusted for gender and age, we found that those who were outside of the reference range of peripheral blood lymphocytes (NK cell, B cell, CD3+ T cell and CD3+CD4+ T cell) had an increased risk of PD [odds ratio (OR): 2.3, 5.1, 3.1 and 4.1, P<0.05, respectively]. Through a multivariable linear regression model adjusted for gender, age and levodopa equivalent daily dose, we found that deviation from the reference range of CD3+CD8+ T cells (regression coefficient =3.474, P=0.015), course of disease (regression coefficient =0.411, P=0.004) and the Non-Motor Symptoms Scale (NMSS) scores (regression coefficient =0.553, P=5.92E-11) had a positive association with the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS)-III score (adjusted R2=0.364, F=13.004). CONCLUSIONS: Abnormal peripheral blood lymphocyte subpopulations have clinical relevance for PD.