Anti-CD14 monoclonal antibody [PE]

Aim Alzheimer's disease (AD) is a chronic neurodegenerative disease. Various inflammatory processes account for the pathology of AD, and macrophages in particular have a distinct polarization phenotype related to M1/M2 classification. We aimed to investigate macrophage polarization patterns as an indicator of cognitive function in AD. Methods We recruited 54 non-demented individuals as control and 105 AD patients as experimental groups respectively. Percentages of macrophage (PM2K(+)CD14(+) and PM2K(+)CD14(-)) and macrophage polarization subsets (M1, M2a, M2b, and M2c) were assessed using flow cytometry. All AD patients were classified by dementia severity using clinical Dementia Rating scale (CDR) as CDR 0.5, 1 and >= 2. AD patients had cognitive function evaluation using Mini-Mental State Examination (MMSE) and Cognitive Assessment Screening Instrument (CASI). We compared the macrophage polarization patterns between control and patient groups. Cognitive function was evaluated in association with macrophage polarization patterns in AD patients. Results The percentages of PM2K(+)CD14(+) and PM2K(+)CD14(-) macrophages were higher in AD patients than in controls. M2b macrophage subset decrement and M1 macrophage subset increment of PM2K(+)CD14(+) and PM2K(+)CD14(-) macrophages were observed in AD patients compared with controls. Although percentages of macrophage subsets were not consistent with CDR staging, PM2K(+)CD14(+)M2b macrophage subset decrement was correlated with worse cognitive functioning by MMSE and CASI in AD patients. Conclusion M2b macrophage subset decrement and M1 macrophage subset increment were noted in AD patients, while PM2K(+)CD14(+)M2b macrophage subset decrement indicated worse cognitive function in such patients.

Glucose is the primary osmotic medium used in most peritoneal dialysis (PD) solutions, and long-term exposure to high glucose is a major contributor to peritoneal fibrosis. Our previous study revealed that M2 macrophages participate in the development of PD-related fibrosis in a rat model. In the present study, the effects of high glucose on peritoneal macrophage polarizationin vivoandin vitrowere further evaluated. Continuous ambulatory PD (CAPD) patients with an overnight dwell of 1.5 or 2.5% glucose dialysate were recruited for this study. Overnight effluent samples from patients with CAPD (2,000 ml) were centrifuged to collect cells from the peritoneal cavity. J774A.1 cells (murine macrophages from ascites) were cultured in different concentrations of glucose. Macrophage phenotype markers were detected by flow cytometry. The levels of cytokines in PD effluent and the supernatant of murine macrophages were detected by enzyme-linked immunosorbent assays. The activity of arginase was determined by quantitative colorimetric analysis. In total, 107 CAPD subjects (92 patients using 1.5% glucose dialysate and 15 patients using 2.5% glucose dialysate) were recruited. The percentage of M1 macrophages (CD14- and CCr7-positive cells) in the 1.5 and 2.5% glucose dialysate groups was 23.0 +/- 13.3 and 24.9 +/- 12.0%, respectively. The difference was not significant (P>0.05). The percentage of M2 macrophages (CD14- and CD206-positive cells) in the 1.5% glucose dialysate group (36.2 +/- 11.4%) was significantly decreased compared to the 2.5% glucose dialysate group (43.2 +/- 7.4%) (P<0.05). Murine macrophages were cultured in a high-glucosein vitroenvironment, and the percentage of M1 macrophages in 138.8 mmol/l glucose medium significantly increased over time. The percentage of M2 macrophages increased in a glucose concentration-dependent and time-dependent manner. Arginase 1 in murine macrophages and the level of transforming growth factor beta 1 in the supernatant increased in a glucose concentration-dependent manner. In conclusion, high glucose contributed to the polarization of peritoneal macrophages to the M2 phenotype, which may play an important role in the pathogenesis of PD-related fibrosis.