RESUMO
Studies have shown that eosinophils are closely related to pathogenesis of bronchial asthma. Eosinophils release eosinophil cationic protein (ECP), which plays an important role in infection and allergic reactions. Serum ECP mRNA expression in children with bronchial asthma has not been adequately investigated. We analyzed serum ECP mRNA expression in 63 children with bronchial asthma and 21 healthy children by using reverse-transcriptase polymerase chain reaction to understand the role of ECP in children with bronchial asthma. The children with bronchial asthma were segregated into acute-phase and stable-phase groups, based on the severity of the illness. Serum ECP mRNA expression in children with bronchial asthma (0.375 ± 0.04) was significantly higher than that in healthy controls (0.20 ± 0.02; P < 0.05). Additionally, children in the acute-phase group showed higher ECP mRNA expression level (0.44 ± 0.06) than those in the stable-phase (0.31 ± 0.03) and healthy control groups (0.20 ± 0.02; P < 0.05), while the level in the stable-phase (0.31 ± 0.03) was markedly higher than that in the healthy control group (0.20 ± 0.02; P < 0.05). Detection of serum ECP mRNA expression level has possible applications in the diagnosis and treatment of children with bronchial asthma.
Assuntos
Asma/genética , Proteína Catiônica de Eosinófilo/genética , Eosinófilos/enzimologia , RNA Mensageiro/biossíntese , Asma/sangue , Asma/enzimologia , Hiper-Reatividade Brônquica/sangue , Hiper-Reatividade Brônquica/genética , Criança , Proteína Catiônica de Eosinófilo/biossíntese , Proteína Catiônica de Eosinófilo/sangue , Feminino , Humanos , Masculino , RNA Mensageiro/sangue , RNA Mensageiro/genéticaRESUMO
BACKGROUND: We previously reported that asthmatic children with GSTM1 null genotype may be more susceptible to the acute effect of ozone on the small airways and might benefit from antioxidant supplementation. This study aims to assess the acute effect of ozone on lung function (FEF(25-75)) in asthmatic children according to dietary intake of vitamin C and the number of putative risk alleles in three antioxidant genes: GSTM1, GSTP1 (rs1695), and NQO1 (rs1800566). METHODS: 257 asthmatic children from two cohort studies conducted in Mexico City were included. Stratified linear mixed models with random intercepts and random slopes on ozone were used. Potential confounding by ethnicity was assessed. Analyses were conducted under single gene and genotype score approaches. RESULTS: The change in FEF(25-75) per interquartile range (60 ppb) of ozone in persistent asthmatic children with low vitamin C intake and GSTM1 null was -91.2 ml/s (p = 0.06). Persistent asthmatic children with 4 to 6 risk alleles and low vitamin C intake showed an average decrement in FEF(25-75) of 97.2 ml/s per 60 ppb of ozone (p = 0.03). In contrast in children with 1 to 3 risk alleles, acute effects of ozone on FEF25-75 did not differ by vitamin C intake. CONCLUSIONS: Our results provide further evidence that asthmatic children predicted to have compromised antioxidant defense by virtue of genetic susceptibility combined with deficient antioxidant intake may be at increased risk of adverse effects of ozone on pulmonary function.
Assuntos
Antioxidantes/administração & dosagem , Ácido Ascórbico/administração & dosagem , Asma/genética , Suplementos Nutricionais , Exposição Ambiental/efeitos adversos , Enzimas/genética , Interação Gene-Ambiente , Predisposição Genética para Doença , Ozônio/efeitos adversos , Fatores Etários , Deficiência de Ácido Ascórbico/tratamento farmacológico , Deficiência de Ácido Ascórbico/epidemiologia , Asma/diagnóstico , Asma/enzimologia , Asma/epidemiologia , Asma/fisiopatologia , Asma/prevenção & controle , Criança , Estudos de Coortes , Método Duplo-Cego , Feminino , Glutationa S-Transferase pi/genética , Glutationa Transferase/genética , Humanos , Modelos Lineares , Pulmão/fisiopatologia , Masculino , Fluxo Máximo Médio Expiratório , México/epidemiologia , NAD(P)H Desidrogenase (Quinona)/genética , Fenótipo , Polimorfismo Genético , Medição de Risco , Fatores de Risco , Saúde da População UrbanaRESUMO
OBJECTIVE: To determine whether a short-term protocol using subcutaneous sensitization with ovalbumin, without the use of adjuvants, would induce an eosinophilic response in the lungs of mice similar to that observed in previous, well-established protocols. METHODS: Adult female BALB/c mice were randomized and divided into groups according to the number of sensitizations with ovalbumin and the number/dosage of intranasal ovalbumin challenges. The short-term protocol (10 days) consisted of one sensitization with ovalbumin and three ovalbumin challenges (100 µg). Total and differential cell counts in BAL fluid, levels of eosinophil peroxidase in lung tissue, and histopathological examination of the lungs were performed 24 h after the last ovalbumin challenge. RESULTS: No significant differences were found among the groups regarding the variables studied. The short-term protocol, as well as the other protocols studied, induced an eosinophilic response similar to that obtained in the positive control. CONCLUSIONS: Subcutaneous sensitization with ovalbumin and without the use of adjuvants resulted in a significant allergic response in the lungs of mice, even in the short-term protocol group. Our findings suggest that this short-term protocol can be used as a first-line pre-clinical test for the study of new medications, reducing the costs and observation periods.
Assuntos
Asma/patologia , Hiper-Reatividade Brônquica/patologia , Peroxidase de Eosinófilo/metabolismo , Pulmão/patologia , Ovalbumina , Eosinofilia Pulmonar/imunologia , Doença Aguda , Animais , Asma/enzimologia , Hiper-Reatividade Brônquica/enzimologia , Testes de Provocação Brônquica , Líquido da Lavagem Broncoalveolar/citologia , Modelos Animais de Doenças , Feminino , Pulmão/enzimologia , Camundongos , Camundongos Endogâmicos BALB C , Eosinofilia Pulmonar/patologia , Distribuição AleatóriaRESUMO
OBJETIVO: Determinar se um protocolo curto de sensibilização com ovalbumina subcutânea, sem adjuvante, induziria uma resposta pulmonar eosinofílica em pulmões de camundongos similar àquela encontrada em protocolos previamente estabelecidos. MÉTODOS: Fêmeas adultas de camundongos BALB/c foram randomizadas e divididas em grupos de acordo com o número de sensibilizações com ovalbumina e o número/dosagem de provocação intranasal. O protocolo curto (10 dias) consistiu de uma sensibilização e três provocações com ovalbumina (100 µg). A contagem total e diferencial de células no lavado broncoalveolar, o nível de peroxidase eosinofílica no tecido pulmonar e o exame histopatológico dos pulmões foram realizados 24 h após a última provocação. RESULTADOS: Não houve diferenças significativas entre os grupos em relação às variáveis estudadas. O protocolo curto, assim como os outros protocolos estudados, induziu uma resposta eosinofílica pulmonar semelhante àquela do grupo controle positivo. CONCLUSÕES: A sensibilização por ovalbumina subcutânea sem o uso de adjuvante resultou em uma significativa resposta pulmonar alérgica em ratos, mesmo no grupo de protocolo curto. Nossos achados sugerem que esse protocolo curto pode ser utilizado como teste pré-clínico de primeira linha para a pesquisa de novos fármacos, reduzindo custos e o tempo de observação.
OBJECTIVE: To determine whether a short-term protocol using subcutaneous sensitization with ovalbumin, without the use of adjuvants, would induce an eosinophilic response in the lungs of mice similar to that observed in previous, well-established protocols. METHODS: Adult female BALB/c mice were randomized and divided into groups according to the number of sensitizations with ovalbumin and the number/dosage of intranasal ovalbumin challenges. The short-term protocol (10 days) consisted of one sensitization with ovalbumin and three ovalbumin challenges (100 µg). Total and differential cell counts in BAL fluid, levels of eosinophil peroxidase in lung tissue, and histopathological examination of the lungs were performed 24 h after the last ovalbumin challenge. RESULTS: No significant differences were found among the groups regarding the variables studied. The short-term protocol, as well as the other protocols studied, induced an eosinophilic response similar to that obtained in the positive control. CONCLUSIONS: Subcutaneous sensitization with ovalbumin and without the use of adjuvants resulted in a significant allergic response in the lungs of mice, even in the short-term protocol group. Our findings suggest that this short-term protocol can be used as a first-line pre-clinical test for the study of new medications, reducing the costs and observation periods.
Assuntos
Animais , Feminino , Camundongos , Asma/patologia , Hiper-Reatividade Brônquica/patologia , Peroxidase de Eosinófilo/metabolismo , Pulmão/patologia , Ovalbumina , Eosinofilia Pulmonar/imunologia , Doença Aguda , Asma/enzimologia , Testes de Provocação Brônquica , Hiper-Reatividade Brônquica/enzimologia , Líquido da Lavagem Broncoalveolar/citologia , Modelos Animais de Doenças , Pulmão/enzimologia , Camundongos Endogâmicos BALB C , Eosinofilia Pulmonar/patologia , Distribuição AleatóriaRESUMO
Exposure to environmental tobacco smoke (ETS) during early childhood increases the risk of developing asthma. The intention of this study was to genotype a population of children from Coahuila state in Northern Mexico and to determine whether polymorphisms of the CYP1A1, GSTP1, and IL13 genes are associated with exposure to ETS and subsequently a higher risk for asthma. IL13 plays an important role in the development of allergic response, particularly those related with airway inflammation. CYP1A1 and GSTP1 are xenobiotic-metabolizing enzymes induced by repeated exposure to toxicants. Polymorphisms of these genes have been related with ETS exposure and increased risk for asthma. To assess the effect of IL13 (-1112 C>T and Arg110Gln), GSTP1 (Ile105Val), and CYP1A1 (Ile462Val) on asthma risk and ETS exposure, we recruited 201 unrelated children and classified them into four groups: (1) control without ETS exposure; (2) control with ETS exposure; (3) with asthma and with ETS exposure and (4) with asthma and without ETS exposure. No association among ETS exposure, asthma, and the studied polymorphisms was denoted by multivariate analysis of this population.
Assuntos
Asma/genética , Citocromo P-450 CYP1A1/genética , Interação Gene-Ambiente , Glutationa S-Transferase pi/genética , Interleucina-13/genética , Polimorfismo Genético , Poluição por Fumaça de Tabaco/efeitos adversos , Fatores Etários , Asma/enzimologia , Asma/imunologia , Estudos de Casos e Controles , Distribuição de Qui-Quadrado , Criança , Feminino , Predisposição Genética para Doença , Humanos , Modelos Logísticos , Masculino , México , Análise Multivariada , Razão de Chances , Medição de Risco , Fatores de RiscoRESUMO
Matrix metalloproteinases (MMPs) are crucial to the development and maintenance of healthy tissue and are mainly involved in extracellular matrix (ECM) remodeling of skeletal muscle. This study evaluated the effects of chronic allergic airway inflammation (CAAI), induced by ovalbumin, and aerobic training in the MMPs activity in mouse diaphragm muscle. Thirty mice were divided into 6 groups: 1) control; 2) ovalbumin; 3) treadmill trained at 50% of maximum speed; 4) ovalbumin and trained at 50%; 5) trained at 75%; 6) ovalbumin and trained at 75%. CAAI did not alter MMPs activities in diaphragm muscle. Nevertheless, both treadmill aerobic trainings, associated with CAAI increased the MMP-2 and -1 activities. Furthermore, MMP-9 was not detected in any group. Together, these findings suggest an ECM remodeling in diaphragm muscle of asthmatic mice submitted to physical training. This result may be useful for a better understanding of functional significance of changes in the MMPs activity in response to physical training in asthma.
Assuntos
Asma/reabilitação , Diafragma/metabolismo , Condicionamento Físico Animal , Animais , Asma/enzimologia , Asma/fisiopatologia , Diafragma/enzimologia , Modelos Animais de Doenças , Matriz Extracelular/metabolismo , Masculino , Metaloproteinase 1 da Matriz/metabolismo , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/metabolismo , Camundongos , Camundongos Endogâmicos BALB C , Músculo Esquelético/enzimologia , Músculo Esquelético/metabolismo , OvalbuminaRESUMO
PURPOSE OF REVIEW: The review characterizes airway remodelling in childhood asthma and describes how early in life it is possible to detect, and possibly cure, the cellular and biochemical changes that characterize this event. This topic is timely and relevant since a variety of clinical and epidemiologic studies strongly suggest that in asthma, remodelling may start very early in life and that current prevention and treatment measures, including early avoidance measures and pharmaceutical interventions, are relatively ineffective in preventing the development of irreversible airway changes or in reverting them, once established. RECENT FINDINGS: Recent findings show that structural changes characterizing remodelling, such as subepithelial basement membrane thickening, epithelial cell disruption, protease/antiprotease imbalance and neoangiogenesis, are detectable in children with asthma and even in children with respiratory symptoms or with atopy, before a clear clinical diagnosis of bronchial asthma is made. SUMMARY: Identification of the early structural changes that may precede the development of asthma and of factors leading to permanent loss of lung function appear central to future asthma management.
Assuntos
Asma/patologia , Sistema Respiratório/patologia , Adolescente , Asma/enzimologia , Criança , Pré-Escolar , Humanos , Lactente , Peptídeo Hidrolases/metabolismo , Sistema Respiratório/enzimologiaRESUMO
In the present study we investigated the lymphocytes infiltration and other parameters of allergic lung inflammation comparing mice submitted to acute suppression of nitric oxide synthesis with mice deficient in inducible nitric oxide synthase (NOS2-/-) gene. At weekly intervals C57Bl/6 mice, wild type and NOS2-/- were sensitized twice with ovalbumin-alumen and challenged twice with ovalbumin aerosol and lungs examined 24 h later. In wild type mice, treatment with nitric oxide synthase inhibitor, N(omega)-nitro-L-arginine-methyl-ester (L-NAME) or aminoguanidine (i.p., 30 min before each ovalbumin challenge) caused a significant decrease in bronchoalveolar lavage cell number: eosinophils (90%), lymphocytes NK1.1+ (70%), Tgammadelta+ (50%), CD4+ (55%), CD8+ (60%) and B220+ (65%). Both inhibitors abolished airway hyperreactivity and significantly reduced mucus secretion (L-NAME 64%; aminoguanidine 58%). Surprisingly, in NOS2-/- mice these parameters of allergic lung inflammation were not significantly different when compared with wild type mice. In addition, treatment of NOS2-/- mice with L-NAME or aminoguanidine did not affect these parameters. Thus, acute inhibition of NOS2 activity inhibits asthma-like responses but absence of NOS2 has no affect.
Assuntos
Asma/patologia , Óxido Nítrico Sintase/metabolismo , Animais , Antígenos/análise , Antígenos Ly , Antígenos de Superfície , Asma/enzimologia , Asma/imunologia , Líquido da Lavagem Broncoalveolar/citologia , Broncoconstritores/farmacologia , Antígenos CD4/análise , Antígenos CD8/análise , Inibidores Enzimáticos/farmacologia , Eosinófilos/citologia , Eosinófilos/efeitos dos fármacos , Eosinófilos/imunologia , Citometria de Fluxo , Guanidinas/farmacologia , Lectinas Tipo C , Antígenos Comuns de Leucócito/análise , Contagem de Leucócitos , Pulmão/efeitos dos fármacos , Pulmão/imunologia , Pulmão/patologia , Contagem de Linfócitos , Linfócitos/citologia , Linfócitos/efeitos dos fármacos , Linfócitos/imunologia , Cloreto de Metacolina/farmacologia , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Knockout , NG-Nitroarginina Metil Éster/farmacologia , Subfamília B de Receptores Semelhantes a Lectina de Células NK , Óxido Nítrico Sintase/antagonistas & inibidores , Óxido Nítrico Sintase/genética , Óxido Nítrico Sintase Tipo II , Ovalbumina/imunologia , Proteínas/análiseRESUMO
Asthma results from allergen-driven intrapulmonary Th2 response, and is characterized by intermittent airway obstruction, airway hyperreactivity (AHR), and airway inflammation. Accumulating evidence indicates that inflammatory diseases of the respiratory tract are commonly associated with elevated production of nitric oxide (NO). It has been shown that exhaled NO may be derived from constitutive NO synthase (NOS) such as endothelial (NOS 3) and neural (NOS 1) in normal airways, while increased levels of NO in asthma appear to be derived from inducible NOS2 expressed in the inflamed airways. Nevertheless, the functional role of NO and NOS isoforms in the regulation of AHR and airway inflammation in human or experimental models of asthma is still highly controversial. In the present commentary we will discuss the role of lipopolysaccharides contamination of allergens as key element in the controversy related to the regulation of NOS2 activity in experimental asthma.
Assuntos
Alérgenos/imunologia , Asma/enzimologia , Lipopolissacarídeos/imunologia , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico/biossíntese , Animais , Asma/imunologia , Modelos Animais de Doenças , Ativação Enzimática , HumanosRESUMO
Asthma results from allergen-driven intrapulmonary Th2 response, and is characterized by intermittent airway obstruction, airway hyperreactivity (AHR), and airway inflammation. Accumulating evidence indicates that inflammatory diseases of the respiratory tract are commonly associated with elevated production of nitric oxide (NO). It has been shown that exhaled NO may be derived from constitutive NO synthase (NOS) such as endothelial (NOS 3) and neural (NOS 1) in normal airways, while increased levels of NO in asthma appear to be derived from inducible NOS2 expressed in the inflamed airways. Nevertheless, the functional role of NO and NOS isoforms in the regulation of AHR and airway inflammation in human or experimental models of asthma is still highly controversial. In the present commentary we will discuss the role of lipopolysaccharides contamination of allergens as key element in the controversy related to the regulation of NOS2 activity in experimental asthma.
Assuntos
Animais , Humanos , Alérgenos/imunologia , Asma/enzimologia , Lipopolissacarídeos/imunologia , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico/biossíntese , Asma/imunologia , Modelos Animais de Doenças , Ativação EnzimáticaRESUMO
Asthma is an inflammatory condition characterized by the involvement of several mediators, including reactive oxygen species. The aim of the present study was to investigate the superoxide release and cellular glutathione peroxidase (cGPx) activity in peripheral blood granulocytes and monocytes from children and adolescents with atopic asthma. Forty-four patients were selected and classified as having intermittent or persistent asthma (mild, moderate or severe). The spontaneous or phorbol myristate acetate (PMA, 30 nM)-induced superoxide release by granulocytes and monocytes was determined at 0, 5, 15, and 25 min. cGPx activity was assayed spectrophotometrically. The spontaneous superoxide release by granulocytes from patients with mild (N = 15), moderate (N = 12) or severe (N = 6) asthma was higher at 25 min compared to healthy individuals (N = 28, P < 0.05, Duncan test). The PMA-induced superoxide release by granulocytes from patients with moderate (N = 12) or severe (N = 6) asthma was higher at 15 and 25 min compared to healthy individuals (N = 28, P < 0.05 in both times of incubation, Duncan test). The spontaneous or PMA-induced superoxide release by monocytes from asthmatic patients was similar to healthy individuals (P > 0.05 in all times of incubation, Duncan test). cGPx activity of granulocytes and monocytes from patients with persistent asthma (N = 20) was also similar to healthy individuals (N = 10, P > 0.05, Kruskal-Wallis test). We conclude that, under specific circumstances, granulocytes from children with persistent asthma present a higher respiratory burst activity compared to healthy individuals. These findings indicate a risk of oxidative stress, phagocyte auto-oxidation, and the subsequent release of intracellular toxic oxidants and enzymes, leading to additional inflammation and lung damage in asthmatic children.
Assuntos
Asma/sangue , Glutationa Peroxidase/metabolismo , Granulócitos/enzimologia , Monócitos/enzimologia , Superóxido Dismutase/biossíntese , Adolescente , Asma/enzimologia , Biomarcadores/sangue , Biomarcadores/metabolismo , Estudos de Casos e Controles , Criança , Doença Crônica , Feminino , Humanos , Masculino , Fatores de TempoRESUMO
Asthma is an inflammatory condition characterized by the involvement of several mediators, including reactive oxygen species. The aim of the present study was to investigate the superoxide release and cellular glutathione peroxidase (cGPx) activity in peripheral blood granulocytes and monocytes from children and adolescents with atopic asthma. Forty-four patients were selected and classified as having intermittent or persistent asthma (mild, moderate or severe). The spontaneous or phorbol myristate acetate (PMA, 30 nM)-induced superoxide release by granulocytes and monocytes was determined at 0, 5, 15, and 25 min. cGPx activity was assayed spectrophotometrically. The spontaneous superoxide release by granulocytes from patients with mild (N = 15), moderate (N = 12) or severe (N = 6) asthma was higher at 25 min compared to healthy individuals (N = 28, P < 0.05, Duncan test). The PMA-induced superoxide release by granulocytes from patients with moderate (N = 12) or severe (N = 6) asthma was higher at 15 and 25 min compared to healthy individuals (N = 28, P < 0.05 in both times of incubation, Duncan test). The spontaneous or PMA-induced superoxide release by monocytes from asthmatic patients was similar to healthy individuals (P > 0.05 in all times of incubation, Duncan test). cGPx activity of granulocytes and monocytes from patients with persistent asthma (N = 20) was also similar to healthy individuals (N = 10, P > 0.05, Kruskal-Wallis test). We conclude that, under specific circumstances, granulocytes from children with persistent asthma present a higher respiratory burst activity compared to healthy individuals. These findings indicate a risk of oxidative stress, phagocyte auto-oxidation, and the subsequent release of intracellular toxic oxidants and enzymes, leading to additional inflammation and lung damage in asthmatic children.
Assuntos
Humanos , Masculino , Feminino , Criança , Adolescente , Asma/sangue , Glutationa Peroxidase/metabolismo , Granulócitos/enzimologia , Monócitos/enzimologia , Superóxido Dismutase/biossíntese , Asma/enzimologia , Biomarcadores/sangue , Estudos de Casos e Controles , Doença Crônica , Fatores de TempoRESUMO
Asthma results from an intrapulmonary allergen-driven Th2 response and is characterized by intermittent airway obstruction, airway hyperreactivity, and airway inflammation. An inverse association between allergic asthma and microbial infections has been observed. Microbial infections could prevent allergic responses by inducing the secretion of the type 1 cytokines, IL-12 and IFN-gamma. In this study, we examined whether administration of bacterial LPS, a prototypic bacterial product that activates innate immune cells via the Toll-like receptor 4 (TLR4) could suppress early and late allergic responses in a murine model of asthma. We report that LPS administration suppresses the IgE-mediated and mast cell-dependent passive cutaneous anaphylaxis, pulmonary inflammation, airway eosinophilia, mucus production, and airway hyperactivity. The suppression of asthma-like responses was not due to Th1 shift as it persisted in IL-12(-/-) or IFN-gamma(-/-) mice. However, the suppressive effect of LPS was not observed in TLR4- or NO synthase 2-deficient mice. Our findings demonstrate, for the first time, that LPS suppresses Th2 responses in vivo via the TLR4-dependent pathway that triggers NO synthase 2 activity.
Assuntos
Antialérgicos/administração & dosagem , Asma/imunologia , Asma/prevenção & controle , Lipopolissacarídeos/administração & dosagem , Glicoproteínas de Membrana/fisiologia , Óxido Nítrico Sintase/metabolismo , Receptores de Superfície Celular/fisiologia , Transdução de Sinais/imunologia , Administração por Inalação , Alérgenos/administração & dosagem , Alérgenos/imunologia , Animais , Asma/enzimologia , Asma/genética , Brônquios/metabolismo , Hiper-Reatividade Brônquica/genética , Hiper-Reatividade Brônquica/imunologia , Hiper-Reatividade Brônquica/prevenção & controle , Citocinas/antagonistas & inibidores , Citocinas/biossíntese , Ativação Enzimática/imunologia , Imunidade Inata/genética , Inflamação/embriologia , Inflamação/genética , Inflamação/imunologia , Inflamação/prevenção & controle , Injeções Intravenosas , Interferon gama/fisiologia , Interleucina-12/fisiologia , Pulmão/enzimologia , Pulmão/imunologia , Pulmão/patologia , Glicoproteínas de Membrana/deficiência , Glicoproteínas de Membrana/genética , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Endogâmicos C3H , Camundongos Endogâmicos C57BL , Camundongos Knockout , Muco/metabolismo , Óxido Nítrico Sintase/deficiência , Óxido Nítrico Sintase/genética , Óxido Nítrico Sintase/fisiologia , Óxido Nítrico Sintase Tipo II , Ovalbumina/administração & dosagem , Ovalbumina/imunologia , Anafilaxia Cutânea Passiva/genética , Anafilaxia Cutânea Passiva/imunologia , Receptores de Superfície Celular/deficiência , Receptores de Superfície Celular/genética , Salmonella enterica/imunologia , Transdução de Sinais/genética , Células Th2/imunologia , Células Th2/metabolismo , Receptor 4 Toll-Like , Receptores Toll-LikeRESUMO
The nitric oxide is a reactive gas that is produced of endogenous way by enzymes nitric oxide sintetase. Exist a great nitric oxide production induced by the isoforms of the enzyme nitric oxide sintetase, that gives as a result the products training citotoxic, they are important mediating of the defence mechanisms and of normal inflammatory response. The nitric oxide can be detected in the air exhaled in human, their concentrations are increased in patient with asthma, and after the exposition to allergens. The measurement of the exhaled nitric oxide is effected by simple methods, not invasive, to value the degree of inflammation of the air route and response to the treatment with steroids in pediatric patients.
Assuntos
Asma/diagnóstico , Asma/enzimologia , Óxido Nítrico/metabolismo , Biomarcadores , Testes Respiratórios , Criança , Humanos , Óxido Nítrico/análise , Óxido Nítrico/fisiologiaRESUMO
Se describen los niveles de IgE sérica en una muestra de 69 niños con diagnóstico de asma bronquial, de la meseta central de Costa Rica, así como de 33 niños aparentemente sanos, sin historia clínica de alergias, y de 20 adultos donadores de sangre. La comparación mostró un mayor promedio de IgE sérica en el grupo de niños asmáticos con respecto al grupo control, así como una mayor frecuencia de niveles de IgE muy aumentados (>1000 kU/l) en los niños asmáticos. Los valores de IgE hallados en los niños aparentemente sanos son más similares a los descritos en poblaciones de países tropicales que de países de Europa y Norteamérica. Se realizó una comparación entre un método inmunoenzimático y uno radioinmune para la cuantificación de IgE y se obtuvo un coeficiente de correlación de 0,947
Assuntos
Asma/enzimologia , Imunoglobulinas , Costa Rica , Técnicas Imunoenzimáticas , Hipersensibilidade Respiratória/etiologiaRESUMO
A pathogenic role and abnormal function have both been ascribed to the blood platelet in allergy, but the explanation for these observations is unknown. This study compared the cation-stimulated adenosine triphosphatase enzyme (ATPase) activities of platelets from allergic (n = 18), potentially allergic (asymptomatic, positive skin test, n = 5) and normal patients (n = 10), all of whom were without symptoms at the time of the study. Platelets were separated by centrifugation, were sonicated, and were assayed for cation-dependent ATPase activity by spectrophotometry. The mean Na+,K(+)-ATPase activity (in nanomoles per microgram protein per minute) of allergic subjects (0.94 +/- 1.28) was significantly lower than that of normal subjects (3.93 +/- 1.58). No Na+,K(+)-ATPase activity was detectable in platelets from eight of the allergic subjects. The Na+,K(+)-ATPase activity of potentially allergic subjects was intermediate between those of the allergic and normal subjects. A significant negative correlation (p less than 0.01) was observed between serum IgE levels and platelet Na+,K(+)-ATPase values, thus suggesting a relationship between the reduced platelet Na+,K(+)-ATPase and IgE immunoglobulin. No such differences were observed for the Ca+(+)- and Mg+(+)-stimulated ATPases. In vivo dysfunction of the plasma membrane Na+,K(+)-ATPase enzyme in allergic subjects could have profound effects on levels of intracellular cations and thus platelet activation and function.