Adherent endotoxin mediates biological responses of titanium particles without stimulating their phagocytosis
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Abstract Aseptic loosening of orthopaedic implants is thought to be primarily due to stimulation of cytokine production by wear particles from the implants. The cytokines increase osteoclast differentiation, leading to osteolysis and implant loosening. Accumulating evidence indicates that adherent endotoxin mediates the biological responses induced by the wear particles. One mechanism by which adherent endotoxin may act is by increasing phagocytosis of the wear particles. To test this hypothesis, the effect of adherent endotoxin on phagocytosis of titanium particles was determined. First, we developed reliable confocal and fluorescence microscopy methods to examine both the attachment and internalization steps of phagocytosis. Use of these methods showed that adherent endotoxin does not detectably alter the rate or the extent of phagocytosis of titanium particles by RAW 264.7 cells. Despite this lack of an effect on phagocytosis, adherent endotoxin dramatically increases the ability of RAW 264.7 cells to produce TNF‐α and induce osteoclast differentiation. Thus, adherent endotoxin mediates these biological responses by a mechanism that does not rely on increased phagocytosis. These results also demonstrate that phagocytosis is not sufficient to induce cytokine production and osteoclast differentiation but do not rule out the possibility that phagocytosis is required for induction of these responses by titanium particles with adherent endotoxin. © 2002 Orthopaedic Research Society. Published by Elsevier Science Ltd. All rights reserved.Keywords:
Osteolysis
Internalization
Cardioprotection
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In the article there have been discussed the consequences of Listeria internalization and phagocytosis depending on hepatocyte and macrophage receptors type (Met, gC1q-R, C3b-R, Fc-R). It has been supposed that internalization and phagocytosis variant depended on the stage (inductive stage, IgM synthesis stage, IgG synthesis stage) of immunogenesis developing during an infectious process. It has been stated that internalization and phagocytosis mechanism was alternative and defined the destiny of a causative agent in hepatocyte and macrophage as well as the possibility of granulomas formation and of their reverse development.
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Abstract Particle‐induced osteolysis is a major issue, and it is most likely the result of enhanced osteoclast activation in the pathogenesis of various skeletal diseases. This study investigated whether the inhibitory effect that Polycan has on osteoclast differentiation can be used to treat osteolysis induced by titanium (Ti) particles. To this end, the effects of Polycan were examined in terms of the cytotoxicity, osteoclast differentiation, cytokine expression, and Ti‐induced calvarial osteolysis. Polycan had no significant cytotoxic effects on bone marrow macrophages (BMMs) but instead increased BMM proliferation. High levels of interleukin (IL)‐6, IL‐12, and macrophage colony‐stimulating factor (M‐CSF) were expressed in BMM cells in the presence of Polycan, suggesting that Polycan drives the differentiation of BMMs into M1 macrophages. Polycan significantly inhibited osteoclast differentiation induced by M‐CSF and the receptor activator of nuclear factor kappa‐B ligand (RANKL). The expression levels of the osteoclast marker genes significantly decreased, and Polycan induced and maintained the expression of IL‐12, which suppressed osteoclast differentiation. In contrast, the RANKL signaling pathway was not inhibited by Polycan. An in vivo calvarial osteolysis model revealed that Polycan significantly decreased the osteoclast numbers and suppressed osteolysis. Our results suggest that the natural compound Polycan is a good candidate for therapeutic intervention against enhanced osteoclast differentiation and Ti particle‐induced osteolysis. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1170–1175, 2016.
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Abstract Macrophages infected in vitro with murine cytomegalovirus (MCMV) manifest depressed phagocytic uptake of a variety of particles within hours after the initiation of infection. Analysis of kinetics of uptake of radiolabeled Staphylococcus aureus by MCMV-infected macrophages indicates that the diminished uptake results from a depression in the calculated maximum velocity of uptake (Vmax) with the apparent Michaelis constant (KM) remaining unaltered. This pattern of altered uptake is typical of that seen after manipulations that affect the surface interactions of macrophages with ingestible particles. Coincubation of macrophages and radiolabeled Staphylococcus with opsonizing antibody resulted in normalization of the phagocytic rates. The surface localization of the defective phagocytosis was further confirmed by light and scanning electron microscopy of the macrophages incubated with Staphylococcus or latex spherules. These data indicate that defective macrophage phagocytosis induced by MCMV infection results from an aberration in the macrophage surface that interferes with the initial macrophage-particle interactions that initiate nonimmune phagocytosis.
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In this study, we determine its macrophage phagocytosis in different growth stage of Avian broiler after absorbed water soluble alfalfa polysaccharides (WSAP) by three kinds of method. The result showed: effect of WSAP on the macrophage phagocytosis in broilers isn't obvious, but individual group's effect is obvious.
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Abstract The cellular mechanism through which osseous breast cancer metastases induce the focal destruction of bone (tumor osteolysis) is unknown. An athymic mouse model designed for the study of tumor osteolysis was developed and the influence of two human breast cancer tumors on bone was studied. Tumor‐induced osteolysis occurred between 7 and 10 weeks after inoculation of mouse femora with MDA‐MB‐231 or MDA‐MB‐435s breast cancer cells. An increase in osteoclast number and an increase in osteoclast size (area) were detected when tumor‐bearing and sham‐injected limbs were compared. In vitro analysis of the influence of the tumor‐conditioned medium on osteoclast‐mediated bone resorption revealed that this conditioned medium stimulated the resorption by increasing both the number of osteoclasts bound to bone and the number of bone resorption pits formed per osteoclast. In addition, in vitro analysis of the influence of breast cancer tumor cells on osteoclast formation or survival, or both, demonstrated that breast cancer cells induced a dramatic increase in the number of osteoclasts detected in culture. Taken in total, these findings suggest that human breast cancer tumors induce osteolysis by enhancing osteoclast adherence to bone, stimulating osteoclast‐mediated bone resorption, and either prolonging the survival of osteoclasts or increasing osteoclast formation.
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Objective To explore the influence of Pseudomonas aeruginosa(PA) biofilm and alginate on macrophage phagocytosis function in mouse.Methods The bacterial biofilm suspension of PA was used to infect macrophage-depleted mouse and control mouse to explore the influence of biofilm on macrophage.The macrophage was isolated from mouse and added with alginate inside,then the phagocytosis rate was determined.The capability of macrophage's phagocytosis was detected by neutral red method.Results The bacterial count in macrophage-depleted mouse compared to the control group was(4.16±3.36)×105 /ml to(5.15±1.92)×105 /ml,t=0.7211,P=0.483.The phagocytosis rate in PA biofilm group compared to the control group was(13.82±4.71)% to(42.73±11.00)%,Q=12.3231,P0.01.This suggested that the PA biofilm group can be more resistant to macrophage phagocytosis compared to the control group.The phagocytosis rate in alginate group compared to the control group was(22.91±6.20)% to(42.73±11.00)%,Q=8.4465,P0.05.This showed that the alginate group can also be more resistant to macrophage phagocytosis compared to the control group.When the concentration of alginate were 0,25,50,75,100,125 and 150 μg/ml the absorbance A(540 nm)which represents the capability of macrophage phagocytosing neutral red,were(0.271±0.044),(0.456±0.062),(0.445±0.061),(0.551±0.065),(0.210±0.053),(0.186±0.026)and(0.195±0.025)respectively.When the alginate's concentration ≤75 μg/ml,the capability of macrophage phagocytosing neutral red strengthened(P0.05),compared to the 0 μg/ml group;When the alginate's concentration 75 μg/ml,the capability of macrophage phagocytosing neutral red decreased(P0.05),compared to the 0 μg/ml group.Conclusion Macrophage can prevent the invasion of PA.PA biofilm can inhibit macrophage phagocytosis.Alginate can promote macrophage phagocytosis at doses of ≤75 μg/ml while larger doses of alginate inhibit macrophage phagocytosis.
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