Taenia crassiceps Antigens Control Experimental Type 1 Diabetes by Inducing Alternatively Activated Macrophages.

Type 1 diabetes (T1D) is an autoimmune disease caused by the selective destruction of the pancreatic ß-cells, causing inability to produce insulin. Proinflammatory cytokines such as IL-1ß, IL-6, TNF-α, IFN-γ, IL-12, IL-17, and NO can be released by CD4 and CD8+ lymphocytes as well as by classically activated macrophages (CAMϕs), which are important in the development of T1D. Helminth infections have been shown to prevent T1D, mainly through Th2-biased responses and increased recruitment of regulatory cell populations. Previously, we have shown that Taenia crassiceps infection in mice significantly reduces hyperglycemia, insulitis, and the incidence of T1D. In this study, we determined whether T. crassiceps-derived products such as soluble (TcS) or excreted/secreted (TcES) antigens might have a beneficial influence on the development of experimental T1D. Treatment with different doses before or after induction of T1D was analyzed. Mice that were pretreated with TcS were unable to develop T1D, whereas those receiving TcES early after T1D induction displayed significantly reduced insulitis and hyperglycemia along with increased recruitment of alternatively activated macrophages (AAMϕs) and myeloid-derived suppressor cells (MDSCs). Finally, we examined the modulatory role of AAMϕs on T1D by depleting macrophages with clodronate-loaded liposomes, demonstrating that AAMϕs are key cells in T1D regulation.

Factores vasculares implicados en la preeclampsia / Vascular factors involved in pre-eclampsia

La preeclampsia es una enfermedad que únicamente se presenta en la mujer embarazada y que se caracteriza por hipertensión y proteinuria con o sin edema después de la semana 20 de embarazo. Aunque se han propuesto múltiples teorías para explicar su patogenia, recientemente éstas han confluido en una circulación placentaria deficiente que ocasiona hipoxia en el producto y disfunción endotelial sistémica en la madre al reducir los factores que promueven un adecuado funcionamiento endotelial. El receptor semejante a FMS 1 (sFlt-1) y la endoglina (sEng) solubles se han asociado a la disminución del factor de crecimiento vascular endotelial (VEGF) y el factor de crecimiento transformante (TGF) en el plasma materno, respectivamente; lo que contribuye a una irrigación deficiente del producto y a alteraciones maternas que conducen a hipertensión y proteinuria. Algunas sustancias como los anticuerpos contra angiotensina II pueden provocar la liberación de tales factores antiangiogénicos. La determinación del sFlt-1 y sEng en el plasma de mujeres embarazadas podrían llegar a utilizarse para predecir qué mujeres padecerán preeclampsia.

Preeclampsia is a disease that only affects pregnant women and is characterized by hypertension and proteinuria with or without edema after 20 weeks' gestation. Although many hypotheses have been postulated to explain its pathogenicity, some of them have recently concurred that the cause may be an altered placental circulation which causes hypoxia to the fetus and systemic endothelium dysfunction to the mother by reducing the factors promoting adequate endothelial functioning. Soluble FMS-like receptor 1 (sFlt-1) and en-doglin (sEng) have been associated to a decrease of Vascular endothelial growth factor (VEGF) and Transforming growth factor (TGF) in mother's plasma, respectively; thus contributing to a deficient persufion of the fetus and to maternal disturbances, leading to hypertension and proteinuria. Some substances like antibodies against angiotensin II may trigger the release of such angiogenic factors. The assessment of sFlt-1 and sEng in pregnant women plasma might be used to to detect those women who will develop preeclampsia.

New insights in endothelial and smooth muscle cell communication.

Based on immunohistochemical techniques against connexins and the intercellular flux of staining molecules, it has previously been shown that electrotonic communication occurs among endothelial and vascular smooth muscle cells, this due to the presence of myoendothelial gap junctions. The aim of this study was to evaluate the density of myoendothelial contacts in the left coronary and internal mammary arteries as well as in the left saphenous vein by means of electron microscopy, the distance between both cells participating in an myoendothelial contact with a semi-automatic image analysis system and the presence of homocellular and heterocellular gap junctions between endothelial and smooth muscle cells by using the immunohistochemical technique and confocal microscopy in thoracic aorta were also analyzed. The results are that all blood vessels studied present myoendothelial contacts, while density studies show that they are more abundant in the saphenous vein. The myoendothelial contact distance is constant and in no case the cytoplasmic processes reach the plasma membrane of the partner cell toward which they are advanced. Homocellular gap junctions were found between smooth muscle cells and between endothelial cells. Heterocellular gap junctions were absent, evidencing the possibility that signaling molecules between endothelial and smooth muscle cells may be transferred through plasma membranes as was once thought and not necessarily by electrotonic communication.