The incidence of anxiety-related diseases is increasing these days, hence there is a need to understand the mechanisms that underlie its nature and consequences. It is known that limbic structures, mainly the prefrontal cortex and amygdala, are involved in the processing of anxiety, and that projections from prefrontal cortex and amygdala can induce activity of the hypothalamic–pituitary–adrenal axis with consequent cardiovascular changes, increase in oxygen consumption, and ROS production. The compensatory reaction can include increased antioxidant enzymes activities, overexpression of antioxidant enzymes, and genetic shifts that could include the activation of antioxidant genes. The main objective of this study was to evaluate the oxidant/antioxidant effect that chronic anxiogenic stress exposure can have in prefrontal cortex, amygdala, and hypothalamus by exposition to predator odor. Results showed (a) sensitization of the HPA axis response, (b) an enzymatic phase 1 and 2 antioxidant response to oxidative stress in amygdala, (c) an antioxidant stability without elevation of oxidative markers in prefrontal cortex, (d) an elevation in phase 1 antioxidant response in hypothalamus. Chronic exposure to predator odor has an impact in the metabolic REDOX state in amygdala, prefrontal cortex, and hypothalamus, with oxidative stress being prevalent in amygdala as this is the principal structure responsible for the management of anxiety.

Entamoeba histolytica trophozoites can induce host cell apoptosis, which correlates with the virulence of the parasite. This phenomenon has been seen during the resolution of an inflammatory response and the survival of the parasites. Other studies have shown that E. histolytica trophozoites undergo programmed cell death (PCD) in vitro, but how this process occurs within the mammalian host cell remains unclear. Here, we studied the PCD of E. histolytica trophozoites as part of an in vivo event related to the inflammatory reaction and the host-parasite interaction. Morphological study of amoebic liver abscesses showed only a few E. histolytica trophozoites with peroxidase-positive nuclei identified by terminal deoxynucleotidyltransferase enzymemediated dUTP nick end labelling (TUNEL). To better understand PCD following the interaction between amoebae and inflammatory cells, we designed a novel in vivo model using a dialysis bag containing E. histolytica trophozoites, which was surgically placed inside the peritoneal cavity of a hamster and left to interact with the host's exudate components. Amoebae collected from bags were then examined by TUNEL assay, fluorescence-activated cell sorting (FACS) and transmission electron microscopy. Nuclear condensation and DNA fragmentation of E. histolytica trophozoites were observed after exposure to peritoneal exudates, which were mainly composed of neutrophils and macrophages. Our results suggest that production of nitric oxide by inflammatory cells could be involved in PCD of trophozoites. In this modified in vivo system, PCD appears to play a prominent role in the host-parasite interaction and parasite cell death. INTRODUCTIONEntamoeba histolytica is the aetiological agent of amoebic dysentery and its main extra-intestinal complication, amoebic liver abscess (ALA). The infection constitutes an important public health problem worldwide, especially in developing countries. The mechanisms by which this parasite causes intestinal and liver tissue damage have been largely defined using various methods, which have been facilitated by the development of different in vivo experimental models of amoebiasis (Tsutsumi & Shibayama, 2006). In the last two decades, multiple studies have been conducted to understand the molecular basis of host-parasite interactions (Ravdin et al., 1989;Leippe et al., 1991;Que & Reed, 2000). The virulence of E. histolytica trophozoites has been considered a multifactorial process governed by specific interactions at the cellular and molecular levels. These host-parasite interactions take place in a series of sequential steps, including adherence (Petri et al., 1987), contact-dependent cytolysis (Huston et al., 2000) and phagocytosis (Orozco et al., 1983). These steps allow the parasite to invade and damage host tissues, as well as to evade detection by the immune system.Programmed cell death (PCD), or apoptosis, has been reported in all multicellular invertebrate and vertebrate lineages; however, various forms of regulated PCD have now been described in u...

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BackgroundThe hemagglutinin-neuraminidase (HN) protein is the major antigenic determinant of the Mumps virus (MuV) and plays an important role in the viral infectious cycle through its hemagglutination/hemadsorption (HA/HD) and neuraminidase (NA) activities. Objective: analyze the biological and immunological properties of a polypeptide derived from a highly conserved region of the HN ectodomain. Methods: a highly conserved region of the HN gene among several MuV genotypes was chosen to be cloned in a eukaryotic expression vector. The pcDNAHN176-construct was transfected into Vero cells and RNA expression was detected by RT-PCR, while the corresponding polypeptide was detected by immunofluorescence and immunochemistry techniques. The HD and NA activities were also measured. The immunogenic properties of the construct were evaluated using two systems: rabbit immunization to obtain sera for detection of the HN protein and neutralization of MuV infection, and hamster immunization to evaluate protection against MuV infection.ResultsA 567 nucleotide region from the HN gene was amplified and cloned into the plasmid pcDNA3.1. Vero cells transfected with the construct expressed a polypeptide that was recognized by a MuV-hyperimmune serum. The construct-transfected cells showed HD and NA activities. Sera from immunized rabbits in vitro neutralized two different MuV genotypes and also detected both the HN protein and the HN176 polypeptide by western blot. Hamsters immunized with the pcDNAHN176-construct and challenged with MuV showed a mild viral infection in comparison to non-immunized animals, and Th1 and Th2 cytokines were detected in them.ConclusionsThe pcDNAHN176-construct was capable of expressing a polypeptide in Vero cells that was identified by a hyperimmune serum anti Mumps virus, and these cells showed the HD and NA activities of the complete MuV HN protein. The construct also elicited a specific immune response against MuV infection in hamsters.

Osteoarthritis is characterised by progressive loss of articular cartilage through the increase of catabolic metalloproteinases, and chondrocyte cytoskeleton disruption has also been reported. In this regard, we studied the effect of Heterotheca inuloides essential oil (HIEO) on the distribution and immunolocalisation of actin, vimentin and tubulin of chondrocytes from cultured rat articular cartilage explants in the presence of the cytoskeleton disassembly agent acrylamide. After 48 h, chondrocytes treated with acrylamide showed changes in actin immunolocalisation and shrinkage, loss of tubulin compartmentalisation and vimentin collapse and redistribution. However, the immunostaining pattern of these three proteins in acrylamide- and HIEO-treated chondrocytes simultaneously retained their typical characteristics. These results suggest that HIEO promotes protein cytoskeleton reorganisation without providing a preventive effect of acrylamide-associated disassembly. However, it is also possible that HIEO prevents vimentin disorganisation by chemical interaction with acrylamide.