Toxicogenomics of the C-C chemokine receptor type 5 (CCR5): Exploring the potential impacts of chemical-CCR5 interactions on inflammation and human health.

This article explores the impact of environmental chemicals on CCR5 expression and related inflammatory responses based on curated data from the Comparative Toxicogenomics Database (CTD). A total of 143 CCR5-interacting chemicals was found, with 229 chemical interactions. Of note, 67 (29.3%) out of 229 interactions resulted in "increased expression" of CCR5 mRNA or CCR5 protein, and 42 (18.3%) chemical interactions resulted in "decreased expression". The top-5 CCR5-interacting chemicals were "Tetrachlorodibenzodioxin", "Lipopolysaccharides", "Benzo(a)pyrene", "Drugs, Chinese Herbal", and "Ethinyl Estradiol". Based on the number of interactions and importance as environmental contaminant, we then focused our analysis on Tetrachlorodibenzodioxin and Benzo(a)pyrene. There is some consistency in the data supporting an increase in CCR5 expression triggered by Tetrachlorodibenzodioxin; although data concerning CCR5-Benzo(a)pyrene interactions is limited. Considering the high linkage disequilibrium between CCR5 and CCR2 genes, we also search for chemicals that interact with both genes, which resulted in 72 interacting chemicals, representing 50.3% of the 143 CCR5-interacting chemicals and 37.5% of the 192 CCR2-interacting chemicals. In conclusion, CTD data showed that environmental contaminants indeed affect CCR5 expression, with a tendency towards increased expression. The interaction of environmental contaminants with other chemokine receptor genes may potentialize their toxic effects on the chemokine system, favoring inflammation.

Examining the paradox of urban disease ecology by linking the perspectives of Urban One Health and Ecology with Cities.

The ecology of zoonotic, including vector-borne, diseases in urban social-ecological systems is influenced by complex interactions among human and environmental factors. Several characteristics contribute to the emergence and spread of infectious diseases in urban places, such as high human population densities, favorable habitat for vectors, and humans' close proximity to animals and their pathogens. On the other hand, urban living can contribute to the improvement of public health through better access to health services and creation of ecological and technological infrastructure that reduces disease burdens. Therefore, urbanization creates a disease ecology paradox through the interplay of urban health penalties and advantages for individual and community outcomes. To address this contradiction, we advocate a holistic Urban One Health perspective for managing urban systems, especially their green spaces and animal populations, in ways that more effectively control the spread of zoonotic diseases. This view should be coupled with an Ecology with Cities approach which emphasizes actionable science needed for urban planning, management and policymaking; developing disease and vector surveillance programs using citizen and community science methods; and improving education and communication actions that help diverse stakeholders understand the complexities of urban disease ecology. Such measures will enable scholars from many disciplines to collaborate with professionals, government officials, and others to tackle challenges of the urban disease paradox and create more sustainable, health-promoting environments.

Selenium reduces bradykinesia and DNA damage in a rat model of Parkinson's disease.

OBJECTIVE: The aim of this study was to explore the effects of selenium (Se) on locomotor activity and DNA damage in a rat model of Parkinson's disease (PD) induced by paraquat (PQ). METHODS: Forty-eight male Wistar rats were divided into four groups: control group (n = 12), Se group (n = 12), PQ group (n = 12), and Se + PQ group (n = 12). PQ was administered intraperitoneally (10 mg/kg). Se was offered in the drinking water at a concentration of 11.18 µg/L. Locomotor activity was evaluated weekly using the narrow beam test. The comet assay was performed to assess the level of DNA damage in leukocytes and in brain cells. RESULTS: As expected, increased DNA damage was found in the PQ group compared with the control and Se groups (P < 0.001). Interestingly, coadministration of Se and PQ effectively prevented the harmful effects of the toxin in locomotor activity and at the molecular level, reducing bradykinesia (P < 0.01) and DNA damage in leukocytes compared with the PQ-only group (P < 0.001), whereas the levels of DNA damage were comparable to those found in the control and Se groups (P > 0.05). Using the comet assay to analyze brain cells, no differences were found between the groups with regard to damage index (P = 0.774), damage frequency (P = 0.817), or non-detectable cell nuclei (P = 0.481). CONCLUSION: In this experimental model of PQ-induced PD, the use of Se could contribute to the maintenance of locomotor activity and the integrity of leukocytes DNA. No changes in the levels of DNA damage in brain cells were observed between the experimental groups.

Influência do estado nutricional de selênio sobre a progressão da infecção pelo HIV / Influence of selenium nutritional status on the progression of HIV infection

Infection by the human immunodeficiency virus (HIV) is a public health problem of global scale, the nutritional status of infected individual shaving a great influence on the progression of HIV infection. In this context, the mineral selenium seems to play an important role. Therefore, this study aimed to discuss the influence of selenium status on HIV infection progression from a literature review. It was found that, among many approaches, in vivo and in vitro studies showed that seleniummay cause changes in health status of HIV patients, as well as suppress virus replication, respectively. However, the results of several studies are contradictory. Thus, we conclude that it is extremely important to develop further studies aiming to elucidate the way in which the effects of selenium can be achieved by improving the diet therapy of patients with HIV.

La infección por el virus de la inmuno deficiencia humana (VIH) es un problema de salud pública de escala global, siendo que el estado nutricional de los individuos infectados por elvirus tiene gran influencia en el desarrollo de la enfermedad. En este contexto, el mineral selenio parece desempeñar un papel destacado. Por lotanto, este estudio tuvo por objetivo discutir la influencia del estado nutricional de selenio en el avance de la infección por el VIH por medio de una revisión de la literatura. Se encontró que, diversos estudios, "in vivo" e "in vitro" muestran que el micronutriente puede ejercer modificaciones en la salud de los portadores de VIH, bien como suprimir la replicación del virus, respectivamente. Pero, los resultados de los estudios muestran contradicciones. Portanto, es importante la realización de más investigación destinada a aclarar la influencia del selenio en la evolución de los pacientes con VIH, lo cual podría ayudar a mejorar el tratamiento dietoterápico de los portadores.

A infecção pelo vírus da imunodeficiência humana (HIV) é um problema de saúde pública de escala global, sendo que o estado nutricional dos indivíduos infectados pelo vírus exerce grande influência na progressão da infecção pelo HIV. Nesse contexto, o mineral selênio parece desempenhar papel de destaque. Com isso, este trabalho teve como objetivo discutir a influência do estado nutricional de selênio sobre a progressão da infecção pelo HIV a partir de revisão da literatura. Verificou-se que, entre muitas abordagens, estudos in vivo e in vitro mostraram que o micronutriente pode exercer modificações no estado de saúde de portadores do HIV, bem como suprimir a replicação do vírus, respectivamente. Porém, os resultados de vários trabalhos se mostram contraditórios. Assim, conclui-se que é de extrema necessidade a realização de mais estudos com o objetivo de elucidar a forma pela qual os efeitos do uso de selênio podem ser alcançados, aprimorando o tratamento dietoterápico dos pacientes portadores do HIV.