BackgroundMacrophages play a dual role in host defence. They act as the first line of defence by mounting an inflammatory response to antigen exposure and also act as antigen presenting cells and initiate the adaptive immune response. They are also the primary infiltrating cells at the site of inflammation. Inhibition of macrophage activation is one of the possible approaches towards modulating inflammation. Both conventional and alternative approaches are being studied in this regard. Ginger, an herbal product with broad anti inflammatory actions, is used as an alternative medicine in a number of inflammatory conditions like rheumatic disorders. In the present study we examined the effect of ginger extract on macrophage activation in the presence of LPS stimulation.MethodsMurine peritoneal macrophages were stimulated by LPS in presence or absence of ginger extract and production of proinflammatory cytokines and chemokines were observed. We also studied the effect of ginger extract on the LPS induced expression of MHC II, B7.1, B7.2 and CD40 molecules. We also studied the antigen presenting function of ginger extract treated macrophages by primary mixed lymphocyte reaction.ResultsWe observed that ginger extract inhibited IL-12, TNF-α, IL-1β (pro inflammatory cytokines) and RANTES, MCP-1 (pro inflammatory chemokines) production in LPS stimulated macrophages. Ginger extract also down regulated the expression of B7.1, B7.2 and MHC class II molecules. In addition ginger extract negatively affected the antigen presenting function of macrophages and we observed a significant reduction in T cell proliferation in response to allostimulation, when ginger extract treated macrophages were used as APCs. A significant decrease in IFN-γ and IL-2 production by T cells in response to allostimulation was also observed.ConclusionIn conclusion ginger extract inhibits macrophage activation and APC function and indirectly inhibits T cell activation.
This study explores graft geometry and hemodynamics in a reproducible canine arteriovenous loop graft model of intimal-medial hyperplasia. Untapered 6 mm diameter polytetrafluoroethylene grafts (n = 10) were paired with 4 to 7 mm taper (n = 5) or 7 to 4 mm taper (n = 5) grafts for a 12-week period. Several hemodynamic variables were assessed at multiple locations, and venous intimal-medial thickness was measured at locations corresponding to the hemodynamic measurements. Color Doppler imaging demonstrated energy transfer out of the vessel in the form of perivascular tissue vibration. This was quantitated by the distance required for Doppler signal attenuation or volume of the detected vibration signal. Differences among graft types were noted for pressure, flow velocity, tissue vibration, and venous intimal-medial thickness. Hyperplasia was significantly decreased in 4 to 7 mm taper grafts. Stepwise deletion regression indicated volume of the vibration signal had a better correlation with venous intimal-medial thickness than any other variable (r 0.9, p less than 0.001). We conclude that graft geometry can have a significant impact on hemodynamic factors and venous intimal-medial hyperplasia in arteriovenous loop grafts. Flow disturbances appear to cause energy transfer through the vessel wall and into perivascular tissue. Kinetic energy transfer in the form of perivascular tissue vibration was quantitated in vivo and correlates strongly with venous intimal-medial thickness.
Our study provides a uniform survey of the immunomodulatory properties of 10 commonly used herbal products and paves the way for testing these effects in vivo and in clinical setting.
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