Oxidative damage in lymphocytes of copper smelter workers correlated to higher levels of excreted arsenic.

Arsenic has been associated with multiple harmful effects at the cellular level. Indirectly these defects could be related to impairment of the integrity of the immune system, in particular in lymphoid population. To characterize the effect of Arsenic on redox status on this population, copper smelter workers and arsenic unexposed donors were recruited for this study. We analyzed urine samples and lymphocyte enriched fractions from donors to determinate arsenic levels and lymphocyte proliferation. Moreover, we studied the presence of oxidative markers MDA, vitamin E and SOD activity in donor plasma. Here we demonstrated that in human beings exposed to high arsenic concentrations, lymphocyte MDA and arsenic urinary levels showed a positive correlation with SOD activity, and a negative correlation with vitamin E serum levels. Strikingly, lymphocytes from the arsenic exposed population respond to a polyclonal stimulator, phytohemaglutinin, with higher rates of thymidine incorporation than lymphocytes of a control population. As well, similar in vitro responses to arsenic were observed using a T cell line. Our results suggest that chronic human exposure to arsenic induces oxidative damage in lymphocytes and could be considered more relevant than evaluation of T cell surveillance.

Regulatory T cells are locally induced during intravaginal infection of mice with Neisseria gonorrhoeae.

Neisseria gonorrhoeae is a gram-negative diplococcus that in human beings produces gonorrhea. Much clinical evidence has led to the conclusion that gonococcus has important mechanisms to evade host immune functions; however, these mechanisms are only now beginning to be elucidated. In this study, we determined that the BALB/c mouse is a good animal model to study gonococcus infection and examined the immune response against the bacteria. We determined that after intravaginal inoculation of mice with Neisseria gonorrhoeae, the bacteria reached and invaded the upper female reproductive tissues and elicited a T-cell-specific immune response associated with a very weak humoral response, altogether resembling gonococcus infection and disease in women. Remarkably, in the draining lymph nodes of the genital tracts of infected mice, we found an increase of regulatory T lymphocytes, namely, transforming growth factor beta1-positive CD4(+) T cells and CD4(+) CD25(+) Foxp3(+) T cells. Altogether, results indicate that N. gonorrhoeae induces regulatory T cells, which might be related to the local survival of the pathogen and the establishment of a chronic asymptomatic infection.

The release of sympathetic neurotransmitters is impaired in aged rats after an inflammatory stimulus: a possible link between cytokine production and sympathetic transmission.

Aging results in a general decline in the response to external insults, including acute inflammatory challenges. In young animals, the inflammatory response requires activation of the sympathetic system, including neurotransmitters such as ATP, and catecholamines (epinephrine and norepinephrine). To test whether aging affects activation of this axis, and whether this in turn might affect cytokine release, we administered lipopolysaccharide (LPS) i.p. to adult, middle-aged and aged Fisher 344 rats (6-, 15- and 23-month old, respectively) and evaluated the early (0-12h) serum levels of Neuropeptide-Y (NP-Y), ATP and vanillyl mandelic acid (VMA, as an indirect measurement of catecholamine levels). In addition, we evaluated the association between these factors and serum levels of the cytokines tumor necrosis factor-alpha (TNFalpha) and interleukin-10 (IL-10). Induction of both ATP and NP-Y was markedly reduced in the serum of aged animals, when compared to their younger counterparts, while induction of VMA was not affected by age. In spite of these changes, serum levels of TNFalpha and IL-10 were strongly hyper induced and delayed in aged rats. The results suggest that during aging there is a dysregulation in sympathetic neurotransmitter regulatory mechanisms, and this might play a role in the impairment of the inflammatory response.

Hambre, miseria y enfermedad en latinoamérica y el caribe: el papel de la nutrición en las enfermedades tropicales desatendidas (ETDs) en nicaragua / Hunger, misery and disease in Latin America and the Caribbean: the role of nutrition in neglected tropical diseases (NTDs) in Nicaragua

La alimentación y la nutrición adecuadas son el primer y el más importante de los derechos humanos fundamentales y de los determinantes de la salud de las personas. Con el propósito de ayudar a reducir el impacto del hambre y facilitar el control y la eliminación de las enfermedades tropicales desatendidas (ETDs), contribuyendo al alcance de la seguridad alimentaria en la población escolar del Departamento de Chinandega (Nicaragua), se desarrolló el proyecto piloto “Hambre, miseria y enfermedad: el papel de la nutrición en las enfermedades tropicales desatendidas (ETDs) en Nicaragua”. El presente artículo documenta esta experiencia. Para conseguir los objetivos planteados se organizó una jornada científica con expertos en nutrición y en las ETDs, un panel elaboró las conclusiones que sirvieron para la redacción del documento de consenso, en el cual se fundamentó la elaboración de los materiales a ser utilizados en la intervención educativa: “Alimentación para crecer sano”, manual dirigido a los promotores de salud y “Manual de estrategias educativas: alimentación para crecer sano” dirigido a los escolares. Se realizaron cuatro jornadas de capacitación que inicialmente involucró a 80 maestros de 20 escuelas, y que en la última jornada logró sumar 145 docentes. Seguidamente se desarrolló la fase de multiplicación en las escuelas, con la participación de 2.327 niños de entre 7 y 14 años de edad. En esta experiencia la receptividad de los docentes, la mejora en sus habilidades y conocimientos son una garantía para la replicación en los niños y niñas(AU)

Food and proper nutrition are the first and most important of fundamental human rights and the determinants of health of people. In order to help reduce the impact of hunger and facilitate the control and elimination of neglected tropical diseases (NTDs), contributing to the extent of food safety in the school population of the Department of Chinandega (Nicaragua), the pilot project “Hunger, misery and disease: the role of nutrition in neglected tropical diseases (NTDs) in Nicaragua” was developed. This article documents this experience. To achieve the goals a scientific conference with experts in nutrition and NTDs was organized, a panel drew conclusions that were used for drafting the consensus document in which the development of the materials was based to be used in the intervention education: A “Food to grow healthy” manual aimed at health promoters and a “Manual of educational strategies: healthy food for growth” aimed at schoolchildren. Four days of training initially involved 80 teachers from 20 schools were made, and on the last day managed to reach 145 teachers. Then the multiplication phase in schools was developed with the participation of 2,327 children between 7 and 14 years old. In this experience the receptivity of teachers, improving their skills and knowledge are a guarantee for replication in children(AU)

Lactation inhibits the potentiating effect of galanin upon the GnRH-induced LH release observed in diestrous-1 rat

Recent demonstrations of no changes in hypothalamic gonadotropin releasing hormone (GnRH) gene expression nd GnRH levels detected at the pituitary gland in diestrous and lactating rats, indicate that lactational hypogonadotropism in this species is not associated with inhibition of hypothalamic GnRH synthesis and secretion. Hypothalamic galanin potentiates GnRH effects on luteinizing hormone (LH) secretion in male and cycling rats. To explore the interaction between GnRH and galanin during lactation, we studied in vitro the effects of pulsatile stimulation with those peptides upon LH synthesis and secretion from rat pituitaries on diestrous 1 or day 10 of lactation. Hemipituitaries were separately incubated in 1 ml Dulbecco's Minimal Essential Medium supplemented with 1 per cent penicillin-streptomycin and fetal calf serum, at 37 degrees Celsius in 5 per cent CO2-air. The hemipituitaries were stimulated during 12 h with hourly pulses, 6 min each, of (a) gonadotropin releasing hormone (GnRH 25 ng/pulse), (b) rat galanin (600 ng/pulse), (c) GnRH plus galanin, or (d) saline. Medium was collected before each pulse to determine LH by radioimmunoassay. After the 12 h pulsatile regime total RNA was extracted and both actin and beta-LH mRNA were determined by reverse transcriptase polymerase chain reaction. There was a significant stimulation of LH secretion by GnRH (ANOVA, p<0.001) without significant differences between diestrous and lactation pituitaries. Galanin alone did not modify LH secretion but it potentiated the effect of GnRH upon pituitaries from diestrous (p=0.036) but not lactating rats. Neither peptide alone or its combination modified pituitary beta-LH mRNA levels. Results show that galanin regulates differently the secretion and synthesis of LH at the pituitary level. The disappearance of galanin-induced potentiation of GnRH effects upon LH secretion during lactation might contribute to the hypogonadotropism of lactation in the rat.