METHODS: Seventeen patients with alcohol dependence admitted for de-addiction treatment and 12 healthy controls were enrolled in the study. Blood samples were collected at baseline, after one-week, and after one-month, and CD200 levels were measured using enzyme-linked immunosorbent assay kit and compared with the healthy controls.
RESULTS: The serum level of the neuroimmune regulatory protein CD200 in alcohol dependent group (at baseline) was significantly lower compared to healthy controls (p=0.003), and increased after one-week, and one-month period.
CONCLUSION: The present study indicates that decrease of CD200 serum levels in alcohol dependent patients and its rise during alcohol withdrawal and abstinence may provide a preliminary evidence of the role of neuroimmune regulatory proteins in neuroadaptation during alcohol withdrawal.
METHODS: Exosomes were isolated by ultracentrifugation and characterized using nanoparticle tracking analysis (NTA), scanning electron microscopy (SEM), and Western blot. The effect of exosomes in modulating monocyte phenotypes as well as cytokine secretion were further assessed in a co-culture condition using flow cytometry and ELISA accordingly.
RESULTS: Exosomes were identified as spherical particles with a size distribution ranging from 30 nm to 150 nm. These nanoparticles intensely expressed exosome protein markers including CD9, CD63, CD81, and HSP70. The expression of HLA-DR, CD14, and CD11b on monocytes decreased in the presence of exosomes after 24 h of incubation, regardless of the dose. Exosomes significantly induced the release of anti-inflammatory cytokines IL-1Ra in a time- and dose-dependent manner, while TNF-α secretion remains unchanged regardless of the presence or absence of exosomes.
CONCLUSION: This study highlights the immunoregulatory role of exosomes on monocytes, emphasizing the need for further studies into the underlying mechanism.
METHODS: EMA detection was performed by flow cytometry in monocytes and monoblasts. EMA expression was compared with other known markers of monocytic-macrophage lineage (CD11c, CD14 and intracellular CD68). Samples of purified monocytes were obtained from 20 healthy volunteers. Twenty-two cases of monocytic AML (M4 and M5) were studied and controls were selected from 20 cases of acute lymphoblastic leukaemia (ALL) and 18 cases of non-monocytic AML (M0, M1, M2, M3, and M7).
RESULTS: EMA was shown to be expressed strongly on the surface of all purified monocytes. EMA expression was observed on blast cells in 18/22 (81.8%) cases of AML M4 and M5, but not in that of non-monocytic AML or ALL. In this study EMA monoclonal antibody has demonstrated a strong association (P<0.001) with all the other known markers of monocytic-macrophage lineage in acute leukaemia subtypes. EMA had also shown 100% specificity and 81.8% sensitivity in the diagnosis of AML M4 and M5.
CONCLUSIONS: The monoclonal antibody EMA (clone E29) is a useful marker in the classification of acute myeloid leukaemia and can be used as a supplementary analysis for the diagnosis of acute leukemia with monocytic involvement.