Social vulnerability and cardiovascular risk factors in adolescents.

BACKGROUND: Social vulnerability can influence in the development of cardiovascular risk factors in adolescents (CRF). For this reason, the objective of our study was to evaluate the presence of CRF in adolescents, according to social vulnerability. METHODS: This is a cross-sectional study with 517 adolescents of both sexes, from 10 to 19 years of age, classified into 2 groups by social vulnerability, according to socioeconomic characteristics collected by means of questionnaires, where adolescents who did not have access to drinking water, sewage network, and adequate per capita income were classified as vulnerable. Anthropometric, biochemical, and blood pressure data were evaluated. Level of physical activity was assessed by an adapted questionnaire, and food intake was assessed by a 3-day food record. Independent T, Mann-Whitney, and χ2 tests were used, according to the scale of measurement of the variables, on the statistical program SPSS, version 25, at a significance level of 5%. RESULTS: Adolescents had median age of 14 (11 to 15) years; 58.4% were female; 32.4% were overweight, and 52.4% were physically inactive in leisure. Mean consumption of ultra-processed food was observed to account for 45.0% of calorie intake. Adolescents classified as vulnerable had lower weight, body mass index, waist circumference, hip circumference, and neck circumference when compared to non-vulnerable adolescents. Both groups had cholesterol concentrations above the normal level. Non-vulnerable adolescents had higher triglyceride concentrations, higher alcohol consumption, and lower fiber intake compared to vulnerable adolescents. CONCLUSIONS: Adolescents with social vulnerability are less likely to have cardiovascular risk factors.

Events associated with susceptibility to invasive Salmonella enterica serovar Typhi in BALB/c mice previously infected with Plasmodium berghei ANKA.

Numerous mechanisms have been proposed to explain why patients with malaria are more susceptible to bloodstream invasions by Salmonella spp., however there are still several unknown critical factors regarding the pathogenesis of coinfection. From a coinfection model, in which an S. enterica serovar Typhi (S_Typhi) was chosen to challenge mice that had been infected 24 h earlier with Plasmodium berghei ANKA (P.b_ANKA), we evaluated the influence of malaria on cytokine levels, the functional activity of femoral bone marrow-derived macrophages and neutrophils, and intestinal permeability. The cytokine profile over eight days of coinfection showed exacerbation in the cytokines MCP-1, IFNγ and TNFα in relation to the increase seen in animals with malaria. The cytokine profile was associated with a considerably reduced neutrophil and macrophage count and a prominent dysfunction, especially in ex vivo neutrophils in coinfected mice, though without bacterial modulation that could influence the invasion capacity of ex vivo S_Typhi obtained from liver macerate in non-phagocyte cells. Finally, irregularities in the integrity of intestinal tissue evidenced ruptures in the enterocyte layer, a presence of mononuclear leukocytes in the enterocyte layer, an increase of goblet cells in the enterocyte layer and a high volume of leukocyte infiltrate in the sub-mucosa were greatly increased in coinfected animals. Increases of mononuclear leukocytes in the enterocyte layer and volume of leukocyte infiltrate in the sub-mucosa were also seen in monoinfected animals with P. berghei ANKA. Our findings suggest malaria causes a disarrangement of intestinal homeostasis, exacerbation of proinflammatory cytokines and dysfunction in neutrophils that render the host susceptible to bacteremia by Salmonella spp.