RESUMO
PURPOSE: The aim of this study was to analyze the relationship between adiposity, cardiometabolic risk and cardiorespiratory fitness (CRF) according to different groups of adiponectin concentration. METHODS: 255 adolescents of both sexes, aged 11-17 years old, participated. Anthropometric and biochemical parameters such as body mass, height, abdominal circumference (AC), waist circumference (WC), fat mass, fat-free mass, total cholesterol (TC), high-density lipoprotein (HDL-c), low-density lipoprotein (LDL-c), triglycerides (TG), glucose, insulin, adiponectin, blood pressure, peak oxygen consumption (VO2peak) were measured. Body mass index (BMI), z-score BMI (BMI-z), triponderal mass index (TMI), waist-to-height ratio (WHtR), homeostasis model to assessment insulin resistance (HOMA-IR), and quantitative insulin sensitivity check index (QUICKI) were calculated. Adiponectin was categorized: low adiponectin concentration (LAC ≤ 5.18 µg/mL-1), intermediate (IAC = 5.18 and 7.63 µg/mL-1) and high (HAC ≥ 7.63 µg/ml-1). RESULTS: LAC showed higher BMI, BMI-z and TMI than the other groups (p < 0.05) and higher AC, WC and WHtR that the HAC (p < 0.05). IAC showed lower values of TC, LDL-c and TG, and the LAC presented the highest values of insulin, HOMA-IR and QUICKI (p < 0.05) to the IAC and HAC. HAC presented the lower VO2peak than the other groups (p < 0.01). BMI, TMI, glucose, insulin, HOMA-IR showed inverse, and QUICKI a direct and weak correlation with adiponectin (p < 0.05). No significant association was found between adiponectin and VO2peak (p > 0.05). CONCLUSION: The LAC group had higher means in the anthropometric variables and the worst results related to insulin resistance and sensitivity. Thus, adiponectin may play an important role in obesity and reduced concentration may be a factor in the development of obesity-associated morbidities.
Assuntos
Aptidão Cardiorrespiratória , Resistência à Insulina , Adolescente , Criança , Feminino , Humanos , Masculino , Adiponectina , Antropometria/métodos , Índice de Massa Corporal , LDL-Colesterol , Glucose , Insulina , Obesidade , Fatores de Risco , Triglicerídeos , Circunferência da CinturaRESUMO
Chagas disease is caused by infection with the protozoan Trypanosoma cruzi. CD8 T-lymphocytes help to control infection, but apoptosis of CD8 T cells disrupts immunity and efferocytosis can enhance parasite infection within macrophages. Here, we investigate how apoptosis of activated CD8 T cells affects M1 and M2 macrophage phenotypes. First, we found that CD8 T-lymphocytes and inflammatory monocytes/macrophages infiltrate peritoneum during acute T. cruzi infection. We show that treatment with anti-Fas ligand (FasL) prevents lymphocyte apoptosis, upregulates type-1 responses to parasite antigens, and reduces infection in macrophages cocultured with activated CD8 T cells. Anti-FasL skews mixed M1/M2 macrophage profiles into polarized M1 phenotype, both in vitro and following injection in infected mice. Moreover, inhibition of T-cell apoptosis induces a broad reprogramming of cytokine responses and improves macrophage-mediated immunity to T. cruzi. The results indicate that disposal of apoptotic CD8 T cells increases M2-macrophage differentiation and contributes to parasite persistence.
Assuntos
Linfócitos T CD8-Positivos/imunologia , Doença de Chagas/imunologia , Proteína Ligante Fas/antagonistas & inibidores , Interações Hospedeiro-Parasita , Imunidade Celular/efeitos dos fármacos , Macrófagos/imunologia , Animais , Anticorpos Neutralizantes/farmacologia , Apoptose/efeitos dos fármacos , Assialoglicoproteínas/genética , Assialoglicoproteínas/imunologia , Linfócitos T CD4-Positivos/efeitos dos fármacos , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/parasitologia , Linfócitos T CD8-Positivos/efeitos dos fármacos , Linfócitos T CD8-Positivos/parasitologia , Comunicação Celular/efeitos dos fármacos , Movimento Celular/efeitos dos fármacos , Doença de Chagas/tratamento farmacológico , Doença de Chagas/genética , Doença de Chagas/parasitologia , Técnicas de Cocultura , Proteína Ligante Fas/genética , Proteína Ligante Fas/imunologia , Regulação da Expressão Gênica , Subunidade p35 da Interleucina-12/genética , Subunidade p35 da Interleucina-12/imunologia , Lectinas Tipo C/genética , Lectinas Tipo C/imunologia , Ativação Linfocitária , Macrófagos/efeitos dos fármacos , Macrófagos/parasitologia , Masculino , Proteínas de Membrana/genética , Proteínas de Membrana/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Fenótipo , Trypanosoma cruzi/crescimento & desenvolvimento , Trypanosoma cruzi/imunologiaRESUMO
Genetic diversity among local accessions and varieties subsidize plant breeding programs, allowing the utilization of existing variability in plants that have already adapted to local climate conditions. An alternative to studying genetic variability is the study of diversity. The aim of this research was to study genetic diversity among sugarcane accessions and varieties used for the production of craft-distilled cachaça (distilled sugarcane alcohol) in the region of Lavras, Minas Gerais, Brazil. Using a one-way design, an experiment was conducted in the municipality of Perdões, Minas Gerais to evaluate 35 regional accessions derived from germplasm collection expeditions and four varieties. Using morphological descriptions of 46 multicategorical sugarcane characteristics, dissimilarity and Tocher cluster method analyses were performed. Based on the results, it was concluded that genetic diversity exists among the accessions evaluated for the target traits.
Assuntos
Saccharum/genética , Brasil , Análise por Conglomerados , Deriva Genética , Variação Genética , Fenótipo , Melhoramento Vegetal , Banco de SementesRESUMO
PURPOSE: The objective was to evaluate the quality of diet and the relationship between protein diet and calciuria in children and adolescents with nephrolithiasis. METHODS: Forty-nine children and adolescents (28 male and 21 female; 10.1 +/- 3.16 years old) with nephrolithiasis were included in study. Diet evaluation was performed over a 3 day period in order to determine nutrient consumption. The analysis of diets were carried out by DietWin Clínico 3.0 software. One 24-hour urine sample was collected for the measurement of calcium. Nutritional status was also assessed by Body Mass Index (BMI). RESULTS: The diet of patients containe insufficient energy and calcium. High levels of protein (69.64 +/- 16.42 gm), mainly animal source (65.81 +/- 11.45%) and low levels of calcium (500.95 +/- 284.64 mg) was observed (95%). Analysis of 24 hour urine samples revealed that 25.0% of the patients presented hypercalciuria. A positive correlation (r = 0.26680) between animal protein intake and calciuria was found, in opposite of vegetable protein and calciuria correlation (r = -0.2675). CONCLUSIONS: Animal protein of the diet has a significant effect in urinary excretion of calcium in patients with nephrolithiasis.
Assuntos
Adolescente , Criança , Pré-Escolar , Feminino , Humanos , Masculino , Cálcio/urina , Dieta , Estado Nutricional/fisiologia , Fenômenos Fisiológicos da Nutrição Infantil/fisiologia , Nefrolitíase/metabolismo , Proteínas Alimentares/administração & dosagem , Índice de Massa Corporal , Inquéritos sobre Dietas , Fenômenos Fisiológicos da Nutrição do Adolescente/fisiologia , Comportamento Alimentar/fisiologia , Ingestão de Energia/fisiologia , Nefrolitíase/urina , Proteínas Alimentares/metabolismoRESUMO
We investigated the role of Fas ligand in murine silicosis. Wild-type mice instilled with silica developed severe pulmonary inflammation, with local production of tumor necrosis factor (TNF)-alpha, and interstitial neutrophil and macrophage infiltration in the lungs. Strikingly, Fas ligand-deficient generalized lymphoproliferative disease mutant (gld) mice did not develop silicosis. The gld mice had markedly reduced neutrophil extravasation into bronchoalveolar space, and did not show increased TNF-alpha production, nor pulmonary inflammation. Bone marrow chimeras and local adoptive transfer demonstrated that wild-type, but not Fas ligand-deficient lung macrophages recruit neutrophils and initiate silicosis. Silica induced Fas ligand expression in lung macrophages in vitro and in vivo, and promoted Fas ligand-dependent macrophage apoptosis. Administration of neutralizing anti-Fas ligand antibody in vivo blocked induction of silicosis. Thus, Fas ligand plays a central role in induction of pulmonary silicosis.
Assuntos
Glicoproteínas de Membrana/fisiologia , Silicose/etiologia , Transferência Adotiva , Animais , Apoptose , Modelos Animais de Doenças , Proteína Ligante Fas , Feminino , Técnicas In Vitro , Transtornos Linfoproliferativos/genética , Transtornos Linfoproliferativos/imunologia , Transtornos Linfoproliferativos/patologia , Macrófagos/patologia , Masculino , Glicoproteínas de Membrana/deficiência , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Mutantes , Neutrófilos/patologia , Quimera por Radiação , Dióxido de Silício/toxicidade , Silicose/genética , Silicose/patologia , Fator de Necrose Tumoral alfa/biossínteseRESUMO
After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease, a debilitating cardiac illness caused by the protozoan Trypanosoma cruzi. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with T. cruzi fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-beta (TGF-beta) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E2/TGF-beta release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it in vivo. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.
Assuntos
Apoptose , Macrófagos/parasitologia , Linfócitos T/fisiologia , Trypanosoma cruzi/crescimento & desenvolvimento , Clorometilcetonas de Aminoácidos/farmacologia , Animais , Células Cultivadas , Doença de Chagas/imunologia , Doença de Chagas/parasitologia , Inibidores de Cisteína Proteinase/farmacologia , Dinoprostona/biossíntese , Dinoprostona/fisiologia , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Necrose , Fagocitose/fisiologia , Putrescina/biossíntese , Putrescina/fisiologia , Receptores de Vitronectina/metabolismo , Linfócitos T/efeitos dos fármacos , Linfócitos T/patologia , Fator de Crescimento Transformador beta/fisiologiaAssuntos
Apoptose/fisiologia , Doença de Chagas/fisiopatologia , Linfócitos/fisiologia , Macrófagos/parasitologia , Fagocitose , Trypanosoma cruzi/crescimento & desenvolvimento , Animais , Apoptose/imunologia , Doença de Chagas/imunologia , Doença de Chagas/parasitologia , Humanos , Ativação de Macrófagos , Macrófagos/imunologiaRESUMO
Infection of BALB/c mice with Trypanosoma cruzi resulted in up-regulated expression of Fas and Fas ligand (FasL) mRNA by splenic CD4+ T cells, activation-induced CD4+ T cell death (AICD), and in Fas: FasL-mediated cytotoxicity. When CD4+ T cells from infected mice were co-cultured with T. cruzi-infected macrophages, onset of AICD exacerbated parasite replication. CD4+ T cells from T. cruzi-infected FasL-deficient BALB gld/gld mice had no detectable AICD in vitro and their activation with anti-TCR did not exacerbate T. cruzi replication in macrophages. However, infection of BALB gld/gld mice with T. cruzi resulted in higher and more prolonged parasitemia, compared to wild-type mice. Secretion of Th2 cytokines IL-10 and IL-4 by CD4+ T cells from infected gld mice was markedly increased, compared to controls. In addition, in vivo injection of anti-IL-4 mAb, but not of an isotype control mAb, reduced parasitemia in both gld and wild-type mice. These results indicate that, besides controlling CD4+ T cell AICD and parasite replication in vitro, an intact Fas: FasL pathway also controls the host cytokine response to T. cruzi infection in vivo, being required to prevent an exacerbated Th2-type immune response to the parasite.
Assuntos
Doença de Chagas/etiologia , Doença de Chagas/imunologia , Glicoproteínas de Membrana/deficiência , Células Th2/imunologia , Trypanosoma cruzi/imunologia , Trypanosoma cruzi/patogenicidade , Animais , Apoptose , Sequência de Bases , Linfócitos T CD4-Positivos/imunologia , Linfócitos T CD4-Positivos/metabolismo , Doença de Chagas/genética , Citocinas/biossíntese , Citotoxicidade Imunológica , Primers do DNA/genética , Proteína Ligante Fas , Feminino , Técnicas In Vitro , Ativação Linfocitária , Masculino , Glicoproteínas de Membrana/genética , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C57BL , Camundongos Mutantes , Parasitemia/imunologia , RNA Mensageiro/genética , RNA Mensageiro/metabolismo , Trypanosoma cruzi/crescimento & desenvolvimento , Receptor fas/genéticaRESUMO
Activation-induced cell death (AICD) of CD4+ T lymphocytes was described in infection with Trypanosoma cruzi, but a role for AICD in modulating parasite spread in host cells has not been investigated. In this study, replication of T. cruzi in vitro in murine macrophage (Mphi) monolayers was investigated. Long term (5 to 13 day) replication of infective (trypomastigote) T. cruzi forms was blocked by supernatants from activated (anti-TCR) CD4+ T cells of infected mice or by rIFN-gamma. However, when CD4+ T cells from infected mice were cocultured with Mphi and activated by anti-TCR, marked exacerbation of trypomastigote growth in Mphi ensued. The deleterious effect required contact between T cells and infected Mphi. Both anti-Fas and TCR activation killed a proportion of CD4+ T cells. Ly-6 activation did not induce AICD and did not exacerbate parasite growth. However, Fas-mediated killing of T cells before Ly-6 activation led to exacerbated parasite growth. Although a minor population, Fas-susceptible cells were the major source of IFN-gamma production by activated T cells. Addition of a neutralizing anti-Fas ligand antibody blocked 50 to 60% of CD4+ T cell AICD and reduced trypomastigote growth in T/Mphi cocultures stimulated by anti-TCR. The results demonstrate that in CD4+ T cells from infected mice, the onset of AICD selectively ablates IFN-gamma production and up-regulates parasite replication in Mphi in vitro. These findings suggest a deleterious role for AICD in T. cruzi infection.