Beyond the reproductive effect of sex steroids: their role during immunity to helminth parasite infections.

During the helminth infections, the immune system tends to be modulated by host's sex hormones. Actually, many studies show the reciprocal relationship between sex steroids, the immune system and the elimination or establishment of helminth parasites. Is well known that innate immune response determines the type of adaptive immune response, so the effects in the innate immune response by hormones may affect subsequent adaptive immunity. The sex steroids as estrogens, progesterone and testosterone regulate growth, differentiation, survival and function of many cell types that could be involved in process like homeostasis and immunity, but also have a direct effect on the helminthes, that may probably be mediated by specific receptors on these parasites. Sex steroids, parasites and immunity are closely connected, and their interconnection is involved in the maintenance of elimination or establishment of helminthes in an immunocompetent host. For that reason, understanding the action's mechanisms of sex steroids on immune cells and its direct effect on helminth parasites is important for further progress in the development of novel therapies for chronic helminth diseases associated to immune dysregulation. In this review, we will describe the effects of sex steroids on the immune response during helminth infections as well as the direct effect in these parasites, and the possible implications of these effects on the incidence of several helminth infections.

Contribution of the residual body in the spatial organization of Toxoplasma gondii tachyzoites within the parasitophorous vacuole.

Toxoplasma gondii proliferates and organizes within a parasitophorous vacuole in rosettes around a residual body and is surrounded by a membranous nanotubular network whose function remains unclear. Here, we characterized structure and function of the residual body in intracellular tachyzoites of the RH strain. Our data showed the residual body as a body limited by a membrane formed during proliferation of tachyzoites probably through the secretion of components and a pinching event of the membrane at the posterior end. It contributes in the intravacuolar parasite organization by the membrane connection between the tachyzoites posterior end and the residual body membrane to give place to the rosette conformation. Radial distribution of parasites in rosettes favors an efficient exteriorization. Absence of the network and presence of atypical residual bodies in a ΔGRA2-HXGPRT knock-out mutant affected the intravacuolar organization of tachyzoites and their exteriorization.

Phytoremediatory effect and growth of two species of Ocimum in endosulfan polluted soil.

Endosulfan is a hazardous organochlorine pesticide banned or restricted in several countries. However, it has been found in the environment and in animal samples. To study a potential way to bioremediate soils contaminated with this pesticide, two plant species of the genus Ocimum were studied: Ocimum basilicum L. and Ocimum minimum L., since they are economically feasible and well adapted to the climatic conditions of the Nayarit zone (Mexican pacific coast). Young plants were transplanted into soil experimentally polluted with endosulfan. Growth of both species was not affected by endosulfan, the plants grew, flourished, and produced seeds; 30 days later, endosulfan concentration was lower in the soil with O. basilicum than in the soil without plants. On day 90, no differences in endosulfan concentrations were found between soil with or without O. minimum. At day 1, plants in the polluted soil showed lipoperoxidation, as measured by thiobarbituric acid-reactive species (TBARS). Interestingly, a higher TBARS value was observed at day 3 in transplanted plants as compared to non-transplanted plants. In conclusion, both species can endure endosulfan pollution (as high as 1 g kg(-1)) in soils. O. basilicum seems to be an adequate candidate for bioremediation of soils polluted with endosulfan.