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The experiment was performed on 20 adult Wistar rats aged 12 weeks, divided into two equal groups (control and experimental), each comprised of five males and five females. From the first day of the experiment, the experimental group rats were fed Murigran feed supplemented with ß-l,3/l,6-D-glucan at a dosage of 12-19 mg/rat/d, subject to body weight, while the control- group was administered the same feed without any additives. At the beginning of the experiment and then after 14 days, arterial blood samples were collected from the rats and diluted with heparin to measure and compare the phagocytic activity and oxidative metabolism of peripheral blood granulocytes and monocytes by flow cytometry. Statistically higher levels of the activity were observed in the group of rats administered glucan than in controls, expressed in terms of the percentage of phagocytic cells as well as average fluorescence intensity. ß-l,3/l,6-D-glucan also had a positive effect on the oxidative metabolism of both granulocytes and monocytes after stimulation with E. coli, and on the oxidative metabolism of granulocytes after stimulation with PMA.
The aim of the study was to evaluate the function of monocytes in children with leukemias and lymphomas based on the expression of critical costimulatory, activatory and adhesion molecules (CD80, CD86, HLA-DR and CD54 = ICAM-1), esti­mated with tricolor flow cytometry. In comparison to the control group we found a lower percentage of monocytes with costimulatory molecules (CD80 before and CD86 after lipopolysaccharide stimulation) at the time of diagnosis and of monocytes with HLA-DR molecules after remission induction. We also noted a lower percentage of monocytes with HLA-DR expression in the group with severe or ther­apy resistant infections. The results of our investigation suggest some defect in costimulation and antigen presentation in lymphoproliferative diseases in children.
C-reactive protein (CRP) has two structurally distinct isoforms, the CRP pentamer and the CRP monomer. A role for the CRP monomer in atherosclerosis is emerging, but the underlying mechanisms are only beginning to be understood. Monocytes are an important contributor to atherosclerosis, and foam cell formation is the hallmark of atherogenesis. However, whether the CRP monomer can directly interact with the monocytes and modulate their responses remains unknown. Furthermore, although FcγRIII (CD16) has been identified as the receptor for the CRP monomer on neutrophils, its role in mediating the CRP monomer’s biological effects in other cell types has been questioned. In this study, we investigated the interaction of the CRP monomer with the monocytes using the U937 monocytic cell line. The CRP monomer specifically binds to U937 cells. This binding is unique in that it is independent of FcγRs and insensitive to protease digestion of the cell surface proteins. Further assays revealed that the CRP monomer directly incorporates into the plasma membrane. Interestingly, the presence of the CRP monomer efficiently retards oxidized low-density lipoprotein-induced foam cell formation of PMA-differentiated U937 macrophages and peripheral blood monocytic cell-derived macrophages. These findings provide additional evidence for the notion that the CRP monomer is an active CRP isoform that plays a role in atherogenesis via the direct modulation of the behavior of the monocytes.
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