Browsing by Subject "Inflammatory cells"

Now showing 1 - 4 of 4
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    Changes in MMPs and inflammatory cells in experimental gingivitis
    (Murcia : F. Hernández, 2009) Lorencini, Márcio; Silva, Juliete A.F.; de la Hoz, Cristiane L.R.; Carvalho Hernandes, F.; Stach-Machado Dagmar, R.
    In periodontal disease, extensive disorganization of the extracellular matrix promotes the loss of adhesion between the teeth and periodontium. A previous study suggested a reduction in the area occupied by collagen in the gingiva, during the first week of periodontal disease induction, however, the remaining fibers were more compact and thicker. Therefore, it was decided to investigate which of the MMP-2, -9, -14 and RECK, an MMP inhibitor, were involved in these modifications taking place in early gingivitis induced by ligature. The results of gene expression analysis indicated no changes for RECK. MMP-14 showed a reduction at 7 days of inflammation, and there was an immediate increase in MMP-2 gene expression and enzymatic activity, apparently by the stimulation of resident cells such as fibroblasts. A peak of MMP-9 expression 5 days after ligature followed after the peak of enzymatic activity found two days earlier. This pattern was consistent with the kinetics of macrophage and neutrophil recruitment. Immunohistochemistry suggested that MMP-9 was produced by both resident and inflammatory cells. Based on this evidence, it is suggested that extracellular matrix remodeling is related to MMP-2 and -9 production and activation. This allowed us to conclude that the host inflammatory response represents a significant factor for the advance of periodontal diseases.
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    Fat-rich diet induces inflammatory changes in the intact rat pancreas
    (Murcia : F. Hernández, 1987) Juhani Ramo, O.; Jalovaara, P.; Apaja-Sarkkinen, M.
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    Function of inflammatory cells and neoral cyclosporin-A in heart transplant-associated coronary vasculopathy
    (F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2001) Buján, J.; Jurado, F.; Gimeno, M. J.; Rodriguez, M.; Bellón, J. M.
    The role of Sandimmun Neoral® (S-n) and the immune response in transplant-associated coronary vasculopathy (TACV) was evaluated in a Lewis (Lew)- to-Fischer-344 (F344) rat abdominal heterotopic heart transplant model. Some of the transplant recipients were treated with S-n (5mg/ kg/ day) for 14 days posttransplant, or until sacrifice. Grafts were subjected to immunohistochemical (ED1, CD4, CD8 and a-actin+ cells) anal ysis from day 7 to 100 post-transplant. Singenic controls did not develop TACV, irrespective of whether they had received the drug or not. TACV was detected in Lew-F344 transplants regardless of S-n administration with participation of ED1+, CD8+ and aactin+ cells, although its incidence was lower in animals receiving prolonged S-n treatment. In this model, accelerated arteriosclerosis of the graft appeared to be related more to the rejection effect than to the action of the immunosuppressive agent.
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    Immune response to the long-term grafting of cryopreserved small-diameter arterial allografts
    (F. Hernández y Juan F. Madrid. Universidad de Murcia. Departamento de Biología Celular e Histología, 2012) Rodríguez, M.; Pascual, G.; Pérez-Köhler, B.; Cifuentes, A.; Garcia-Honduvilla, N.; Bellón, J.M.; Buján, J.
    Introduction. The viability and immunological response induced by cryopreserved arterial allografts remain unclear. This study examines the post-graft behaviour of this type of vessel substitute. Materials and methods. Both iliac arteries were extracted from Lewis rats (donors) and used to establish groups of allogeneic fresh (group I) or cryopreserved (group II) grafts in Fisher-344 rats (recipients). Cryopreserved segments for grafting were prepared by automated controlled freezing at a cooling rate of 1°C/min followed by storage in liquid nitrogen vapour at -145°C for 30 days. Before grafting, the vessels were slowly thawed. Animals were sacrificed at 14, 30, 90 and 180 days post-surgery when graft specimens were obtained for light and electron microscopy and immunohistochemical detection of inflammatory cells (CD45, ED1, CD4, CD8). Results. After surgery, 85.71% of the grafts in group I and 82.14% in group II were patent. Following long-term implant, both the fresh and cryopreserved allografts showed complete loss of the muscle compartment of the media. Inflammatory or CD45-positive cells (mainly macrophages and CD8 T-lymphocytes) were detected at earlier time points in suture zones and adventitia. In the fresh allografts, the number of immunolabelled cells steadily increased until they were seen to occupy the entire adventitia at 90 days, with high numbers persisting at 6 months. In the cryopreserved allografts, this adventitial inflammatory infiltrate was significantly reduced. Conclusions. The cryopreservation/slow thawing protocol used diminished the immune response induced by fresh arterial allografts improving their behaviour after grafting.