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nr 3
233-243
EN
The review concerns the susceptibility of human endothelial cells to several viruses, especially CMV and HIV. Viral infections of endothelium in vivo develop usually in immuno-compromissed transplant recipients and in patients with AIDS. Endothelium of noninfected persons presents endogenous, nonspecific immunity against viruses. The constitutive production of cytokines with antiviral activities such as IFN, TNF and IL-6, seems to be responsible for the immunity of endothelium. The consequence of viral infections of endothelium (especially CMV) may be potentiation of allograft rejection and also development of artheriosclerosis. In the article the possible mechanisms and contribution of viruses to the processes are disscussed.
EN
Severe trauma acts as a trigger for the complex cascade of postinjury events leading to the re-lease of different mediators and the development of generalized inflammation. Selectins are a family of adhesion proteins that are responsible for the adherence of polymorphonuclear neu-trophils to the endothelium. This interaction plays an important role in the development of severe complications after multiple trauma. The aim of the present study is to follow the sequential altera-tions in circulating selectins level after severe injury and to evaluate the clinical significance of these mediators in monitoring prognosis and outcome. Thirty four severely traumatized patients were entered into the study. Serum sE-selectin, plasma sP-selectin and sL-selectin concentrations were me-asured and an APACHE II score was calculated on admission to the intensive care unit and during the subsequent 5 days. The patients were divided into survivors and nonsurvivors. Initial soluble P- and E-se-lectin concentrations were significantly elevated in all trauma patients. The highest values of these adhesion molecules were measured in all the observed days in patients with poor prognosis and outcome. In survivors we found a systematic decrease in the sP-selectin concentrations. On admission, the sL-selectin concentrations in all trauma patients were decreased. There were stable, very low values in non-survivors and a slow increase in circulating L-selectin in pa-tients who survived. The pattern of soluble selectins in patients with severe trauma is characterized by increased levels of P- and E-selectin and a decreased concentration of L-selectin. These findings suggest a widespread microvascular en-dothelial activation on injury in the early posttrau-matic period, which may be associated with in-creased neutrophil ? endothelial adhesion, neutrophil extravasation and migration. We sup-pose that these parameters of endothelial cell activation/injury may be useful as another early prognostic factor in severe trauma.
EN
Interleukin 7 (IL)-7 is a pleiotropic, non-redundant cytokine necessary for the development of B and T lymphocytes, in particular gamma delta T cell receptor-positive cell differentiation. The cytokine can function as a cofactor during myelopoiesis and the generation of cytotoxic T cells and natural killer cells, can activate monocytes/macrophages, and support the survival of mature T cells. A role for IL-7 in promoting the formation of Peyer's patch anlage has also been demonstrated. IL-7 is constitutively expressed in the thymus, bone marrow stromal cells, epithelial and dendritic cells, keratinocytes, as well as in fetal and adult liver. IL-7 acts on various cells through its receptor (IL-7R), a heterodimer consisting of an alpha chain (CD127) that specifically binds IL-7 and a common c chain (CD132) shared by other cytokine receptors. The receptor is expressed on bone marrow progenitor cells, lymphoid T and B precursors, and mature T cells. IL-7 activity towards murine endothelial cells has been recently described. The presence of IL-7R on human endothelial cells has also been demonstrated. Several therapeutic applications of recombinant IL-7 have been proposed. These have focused on the enhancement of lymphopoiesis, promotion of stem cell engraftment, and the anti-tumor activity of the cytokine.
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