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Monocyte Activation (monocyte + activation)
Selected AbstractsRole of fibroblasts and fibroblast-derived growth factors in periprosthetic angiogenesisJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 10 2007Miklos Tunyogi-Csapo Abstract The periprosthetic granulomatous soft tissue [designated iterfacial membrane (IFM) in this study] exhibits heterogeneous histopathological features, in which highly vascularized areas with dense cellularity alternate with fibrotic and pseudocapsule-like tissue structures. Although macrophage/monocyte activation is a prominent event in the periprosthetic environment, fibroblasts also phagocytose particulate wear debris both in vivo and in vitro. Particulate wear debris and/or cytokines/growth factors alone or in combination (e.g., in conditioned media of explant cultures of IFMs) stimulated normal synovial and IFM fibroblasts to express inflammatory mediators and growth factors such as interleukin (IL)-1,, IL-6, IL-8, three isoforms of vascular endothelial growth factor (VEGF), monocyte/macrophage chemoattractant protein-1 (MCP-1), macrophage-colony-stimulating factor (M-CSF), cycloxygenases (Cox-1 and Cox-2), acid- and basic-fibroblast growth factors (FGF-1 and FGF-2), leukemia inhibitory factor-1 (LIF-1), transforming growth factor ,-1 (TGF-,1), receptor activator of nuclear factor-kappa B ligand (RANKL), and osteoprotegerin (OPG). Thus, the fibroblast is capable of expressing a wide array of angiogenic and osteoclastogenic factors which are involved in the detrimental processes of the periprosthetic osteolysis. © 2007 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 25:1378,1388, 2007 [source] Fatty acids as metabolic mediators in innate immunityEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 10 2009A. Kopp Abstract Background, Increasing data support the hypothesis of a local and systemic crosstalk between adipocytes and monocytes mediated by fatty acids. The aim of this study was to characterize the immunomodulatory effects of a large panel of fatty acids on cytokines and chemokines in monocytic THP-1 cells and primary human monocytes. We tested whether anti-inflammatory fatty acids are able to inhibit the binding of lipopolysaccharide (LPS) to its receptor, toll-like receptor/MD-2 (TLR4/MD-2). Materials and methods, Resistin, monocyte chemoattractant protein-1 (MCP-1) and tumour necrosis factor (TNF) were measured by enzyme-linked immunosorbent assay. Proteins were analysed by Western blot. A designed Flag-tagged TLR4/MD-2 fusion protein (LPS trap) was used to investigate the effect of fatty acids on binding of LPS to its receptor. In 30 patients with type 2 diabetes mellitus (T2D), the correlation of serum triglyceride levels with LPS-induced monocyte activation was analysed. Results, Eleven fatty acids investigated exerted differential effects on the monocytic release of cytokines and chemokines. Eicosapentaenoic acid had potent anti-inflammatory effects on human primary monocytes and THP-1 cells; 100 and 200 ,M eicosapentaenoic acid dose-dependently inhibited LPS binding to the LPS trap. LPS-induced release of monocytic MCP-1 and TNF was significantly and positively correlated with serum triglyceride levels in 30 patients with T2D. Conclusions, Monocytic activation is differentially regulated by fatty acids and depends on triglyceride levels in T2D. The main finding of the present study shows that eicosapentaenoic acid inhibits the specific binding of LPS to TLR4/MD-2. Eicosapentaenoic acid represents a new anti-inflammatory LPS-antagonist. [source] Activated monocytes and platelet-monocyte aggregates in patients with sickle cell disease*INTERNATIONAL JOURNAL OF LABORATORY HEMATOLOGY, Issue 2 2002TED WUN Tumour necrosis factor-, (TNF-,) and interleukin-1, (IL-1,) increase endothelial surface receptors that mediate the adherence of sickle erythrocytes to the endothelium. Increased circulating levels of these cytokines have been found in patients with sickle cell disease (SCD). Monocytes are a source of both of these inflammatory mediators; we therefore determined whether circulating monocytes were activated in SCD, as defined by intracellular expression of these cytokines. Blood was also assayed for the presence of platelet,monocyte aggregates (PMAs), as platelet adherence is one possible mechanism for monocyte activation. The median percentages of monocytes expressing intracellular TNF-, and IL-1, in SCD patients were 6.8 (2.8,17.3) [median (range)] and 14.1 (1.3,44.8), respectively. In African-American controls the corresponding percentages were 0.3 (0.1,0.5) and 0.4 (0.1,3.0), and in Caucasians 0.2 (0.1,0.5) and 0.8 (0.8,1.9) (P < 0.001, Kruskal,Wallis). The mean percentage (± SD) of PMA was 14.0 ± 8.3 for Caucasian controls, 25.7 ± 7.3 for African-American controls, and 45.7 ± 21.6 for patients with SCD (P < 0.001, RM ANOVA; P < 0.05, Newman,Keuls posthoc test). We conclude that there are increased circulating PMAs and monocyte activation in patients with SCD. [source] Enhanced Biocompatibility in Biostable Poly(carbonate)urethaneMACROMOLECULAR BIOSCIENCE, Issue 4 2004Shan-hui Hsu Abstract Summary: In this work, we synthesized two MDI-based polyurethanes, including a poly(ether)urethane (PEU) and a poly(carbonate)urethane (PCU), by using different soft segments, poly(tetramethylene oxide) and poly(hexyl, ethyl)carbonate diol (,,,2,000). We demonstrated that, in addition to the enhanced biostability of PCU over PEU, the biological performances of PCU in vitro were also improved in general. These included, better cellular attachment and proliferation, less platelet activation, as well as reduced monocyte activation. The unusual wide-ranging enhancement in biocompatibility for PCU was believed to be related to the larger micro-phase separation in PCU (,25 nm) that caused distinct protein adsorption on the surface. The total number of adherent monocytes (nonactivated and activated) on the bare sample surfaces, albumin pre-adsorbed sample surfaces, and fibrinogen pre-adsorbed sample surfaces. [source] Herpes simplex virus type 1 dysregulates anti-fungal defenses preventing monocyte activation and downregulating toll-like receptor-2MICROBIOLOGY AND IMMUNOLOGY, Issue 12 2008Claudio Cermelli ABSTRACT We investigated the interplay occurring between pathogens in the course of dual infections, using an in vitro model in which the THP-1 monocytic cell line is first infected with HSV-1 and then exposed to Ca or Cn. These three pathogens share some pathogenic features: they cause opportunistic infections, target macrophages and are neurotropic. Here, we show that HSV-1-infected THP-1 cells exhibited augmented phagocytosis against the two opportunistic fungi but reduced capability to counteract fungal infection: the better ingestion by monocytes was followed by facilitated fungal survival and replication. Reduced IL-12 production was also observed. Cytofluorimetric analysis showed that HSV-1-infected monocytes exhibit: (i) downregulated TLR-2 and TLR-4, critical structures in fungal recognition; (ii) reduced expression of CD38 and CD69, known to be important markers of monocyte activation; and (iii) enhanced expression of apoptosis and necrosis markers, in the absence of altered cell proliferation. Overall, these findings imply that HSV-1 infection prevents monocyte activation, thus leading to a significant dysfunction of the monocyte-mediated anti- Candida response; HSV-1 induced apoptosis and necrosis of monocytes further contribute to this impairment. [source] ORIGINAL ARTICLE: Enhanced Maternal Anti-Fetal Immunity Contributes to the Severity of Hypertensive Disorder Complicating PregnancyAMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 5 2010Li-Ping Liu Citation Liu L-P, Huang W, Lu Y-C, Liao A-H. Enhanced maternal anti-fetal immunity contributes to the severity of hypertensive disorder complicating pregnancy. Am J Reprod Immunol 2010 Problem, The aim of this study was to evaluate how fetal monocyte activation and maternal anti-fetal antigen-specific antibody-secreting cells (ASC) affect the severity of hypertensive disorder complicating pregnancy (HDCP). Method of study, Forty-six healthy third-trimester pregnant women and 20 patients with gestational hypertension, 20 with mild pre-ecalmpsia and another 20 with severe pre-eclampsia were included in the study. Interleukin-6 (IL-6) release from cord blood monocytes was examined by intracellular cytokine staining and flow cytometric analysis. Moreover, the maternal anti-fetal antigen-specific ASC were detected by enzyme-linked immunospot assay. Results, A significantly increased percentage of IL-6-positive monocytes were detected in the cord blood of study groups compared with the controls (P < 0.01). The percentage of IL-6-positive monocytes was increased as the disease progressed (P < 0.05). There were more anti-fetal antigen-specific ASC in the study groups than those in the controls (P < 0.001). Furthermore, the anti-fetal antigen-specific ASC showed difference in gestational hypertensive and severe pre-eclamptic groups (P < 0.05). Conclusion, We conclude that the fetal monocyte activation and the increase in maternal anti-fetal antigen-specific ASC were related to the incidence and severity of HDCP. These results provide both indirect and direct evidence for the occurrence of exaggerated maternal humoral immunity against the fetal antigens in HDCP. [source] Tailored Control and Optimisation of the Number of Phosphonic Acid Termini on Phosphorus-Containing Dendrimers for the Ex-Vivo Activation of Human MonocytesCHEMISTRY - A EUROPEAN JOURNAL, Issue 16 2008Olivier Rolland Abstract The syntheses of a series of phosphonic acid-capped dendrimers is described. This collection is based on a unique set of dendritic structural parameters,cyclo(triphosphazene) core, benzylhydrazone branches and phosphonic acid surface,and was designed to study the influence of phosphonate (phosphonic acid) surface loading towards the activation of human monocytes ex vivo. Starting from the versatile hexachloro-cyclo(triphosphazene) N3P3Cl6, six first-generation dendrimers were obtained, bearing one to six full branches, that lead to 4, 8, 12, 16, 20 and 24 phosphonate termini, respectively. The surface loading was also explored at the limit of dense packing by means of a first-generation dendrimer having a cyclo(tetraphosphazene) core and bearing 32 termini, and with a first-generation dendrimer based on a AB2/CD5 growing pattern and bearing 60 termini. Human monocyte activation by these dendrimers confirms the requirement of the whole dendritic structure for bioactivity and identifies the dendrimer bearing four branches, thus 16 phosphonate termini, as the most bioactive. [source] Early dexamethasone decreases expression of activation markers on neutrophils and monocytes in preterm infantsACTA PAEDIATRICA, Issue 11 2002I Nupponen Aim: To investigate the effects of early dexamethasone administration on activation of circulating neutrophils and monocytes in preterm infants with respiratory distress syndrome requiring treatment with surfactant. Methods: Neonates (n= 30) with respiratory distress were randomized to receive dexamethasone (DEX group, 29.1 ± 1.2 wk, 1223 ± 156 g, n= 15) from the first postnatal day, or to serve as controls (control group, 29.2 ± 1.4 wk, 1250 ± 148 g, n= 15). Dexamethasone was given as a 4 d course (0.5 mg kg,1 on postnatal days 1 and 2, and 0.25 mg kg,1 on days 3 and 4). Polymorphonuclear leucocyte (PMN) and monocyte surface expression of CD11b, L-selectin and CD14 was quantified with flow cytometry, and plasma macrophage-inflammatory protein-1, (MIP-1,) with an enzyme-linked immunosorbent assay. Blood samples were collected on days 1, 2,3 and 5,7. Results: In the DEX group 1/15, and in the control group 7/15 developed bronchopulmonary dysplasia (p < 0.04). PMN CD11b (median 100, range 70-190 vs 154, 96,213, p= 0.01), monocyte CD14 (235, 102,433 vs 355, 219,533, p= 0.01) and plasma MIP-1, (20 ng 1,1, 20,32 vs 37 ng 1,1, 20,70, p= 0.005) were lower in the DEX group at days 2,3. All adhesion molecule expression and plasma MIP-1, levels were comparable at days 5,7, with the exception of monocyte L-selectin expression levels, which remained lower in the DEX group. Conclusion: In preterm infants with respiratory distress syndrome, early dexamethasone causes downregulation of PMN and monocyte activation. This may attenuate pulmonary inflammation and improve pulmonary outcome. [source] | |||||||||||||