Toxoplasma Gondii Infection of Chicken Embryos Causes Retinal Changes and Modulates HSP90B1 Gene Expression: A Promising Ocular Toxoplasmosis Model.

HSP90B1 is a gene that codifies heat shock protein 108 (HSP108) that belongs to a group of proteins induced under stress situation, and it has close relation with the nervous system, especially in the retina. Toxoplasma gondii causes ocular toxoplasmosis that has been associated with a late manifestation of the congenital toxoplasmosis although experimental models show that morphological alterations are already present during embryological development. Here, we used 18 eyes of Gallus domesticus embryos in 7th and 20th embryonic days to establish a model of congenital ocular toxoplasmosis, experimentally infected in its fifth day correlating with HSP90B1 gene expression. Embryos' eyes were histologically evaluated, and gene expression was performed by real-time polymerase chain reaction (PCR). Our data showed parasite present in the choroid, unusual migration of retinal pigment epithelium, and chorioretinal scars, and a tendency to a lower expression of the HSP90B1 gene upon experimental infection. This is a promising model to better understand T. gondii etiopathogeny.

Analysis by Light, Scanning, and Transmission Microscopy of the Intima Synovial of the Temporomandibular Joint of Human Fetuses during the Development.

Objective. To characterize morphologically and ultrastructurally using light microscopy, the scanning electron microscopy and transmission electron microscopy the intima synovial of the temporomandibular joint (TMJ) of human fetuses between the 10th and the 38th week of development. Materials and Methods. The TMJ was dissected bilaterally in 37 human fetuses belonging to the Institute of Embryology of the University Complutense of Madrid and of the Federal University of São Paulo. Results. The outcome by light microscopy showed the morphology of the TMJ and that the formation of inferior joint cavity precedes the superior joint cavity and the presence of blood vessels in the synovial. Conclusion. By scanning and transmission electron microscopy we observed the presence of two well-defined cell types in the intima layer of synovial of the TMJ of human fetuses, macrophage-like type A cell and fibroblast-like type B cell, and the presence of the a third cell type, defined by the name of intermediate lining cell in the intima layer of the synovial.

The involvement of anti-inflammatory protein, annexin A1, in ocular toxoplasmosis.

PURPOSE: The aim of this study was to evaluate the expression of the protein annexin A1 (ANXA1), a potent endogenous regulator of the inflammatory process, in ocular toxoplasmosis. METHODS: C57BL/6 female mice were infected using intravitreal injections of either 10(6) tachyzoites of Toxoplasma gondii (RH strain; T. gondii) or PBS only (control groups). After 24, 48, and 72 h, animals were sacrificed and their eyes were harvested for histopathological, immunohistochemical, and ultrastructural immunocytochemical analysis of ANXA1. Human retinal pigment epithelial (RPE) cells (ARPE-19) were infected in vitro with T. gondii and collected after 60, 120, 240 min, and 24 h. RESULTS: Compared with non-infected eyes, an intense inflammatory response was observed in the anterior (24 h after infection) and posterior segments (72 h after infection) of the infected eye, characterized by neutrophil infiltration and by the presence of tachyzoites and their consequent destruction along with disorganization of normal retina architecture and RPE vacuolization. T. gondii infection was associated with a significant increase of ANXA1 expression in the neutrophils at 24, 48, and 72 h, and in the RPE at 48 and 72 h. In vitro studies confirmed an upregulation of ANXA1 levels in RPE cells, after 60 and 120 min of infection with T. gondii. CONCLUSIONS: The positive modulation of endogenous ANXA1 in the inflammatory and RPE cells during T. gondii infection suggests that this protein may serve as a therapeutic target in ocular toxoplasmosis.