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1.
Rev. patol. respir ; 22(supl.2): S202-S210, jul. 2019. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-188013

RESUMO

La piedra angular del tratamiento de la enfermedad pulmonar obstructiva crónica (EPOC) es la broncodilatación, y en los últimos años se ha desarrollado un importante número de moléculas que han ido cambiando paulatinamente la práctica clínica habitual en estos pacientes. Los fármacos multivalentes con más de un mecanismo de acción broncodilatador representan el próximo paso en materia de relajación del músculo liso bronquial, pero dada la creciente evidencia sobre el estrés oxidativo y estado inflamatorio generalizado de la EPOC, existe una clara tendencia a demostrar el beneficio de formulaciones antiinflamatorias respecto a un potencial control sintomático, y secundariamente la reducción de la importante carga económica que supone el consumo de recursos sanitarios. En este capítulo se pretende dar un resumen esquemático y actualizado sobre los fármacos en investigación en EPOC en las fases previas de su desarrollo clínico


Bronchodilators are the cornerstone of Chronic obstructive pulmonary disease (COPD) treatment, and in the last years an important number of new molecules have changed gradually the clinical practice in these patients. Multivalent drugs with more than one mechanism of action represent the next step in terms of bronchial smooth muscle relaxation, although, giving the growing evidence of oxidative stress and generalized inflammation in COPD, there is a clear tendency to test the potential benefit of new anti-inflammatory drugs for symptoms control in the first place and consequently the reduction of the high economic burden of this disease. This chapter aims to give a schematical and updated review of new drugs for COPD in the preclinical phases of their clinical development


Assuntos
Humanos , Drogas em Investigação/uso terapêutico , Doença Pulmonar Obstrutiva Crônica/tratamento farmacológico , Relaxamento Muscular/efeitos dos fármacos , Broncodilatadores/uso terapêutico , Anticorpos Monoclonais/uso terapêutico , Receptores do Fator de Necrose Tumoral/antagonistas & inibidores , Interleucina-1/antagonistas & inibidores , Interleucina-13/antagonistas & inibidores , Interleucinas/antagonistas & inibidores , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores , Inibidores de Fosfodiesterase/uso terapêutico , Estresse Oxidativo/efeitos dos fármacos
2.
Allergol. immunopatol ; 46(4): 322-325, jul.-ago. 2018. tab, graf
Artigo em Inglês | IBECS | ID: ibc-177862

RESUMO

Introduction and objectives: Atopic dermatitis is a chronic, relapsing, highly pruritic, inflammatory skin disease characterized by typical localization with increasing prevalence of 10-20% in children. Pruritus is one of the major diagnostic criteria of atopic dermatitis and also the main complaint altering quality-of-life of affected patients, inducing and aggravating inflammation. Although pruritus is the absolute symptom of AD, the etiology has not been fully explained yet and current antihistamine therapies are ineffective. The aim of the study was to assess the correlation between IL-31 level and disease severity in patients with atopic dermatitis through Severity SCORing of Atopic Dermatitis (SCORAD) index and the degree of itching assessed subjectively. Material and methods: One hundred thirty-five children were enrolled in the study in total, 70 children with diagnosis of atopic dermatitis and 65 healthy children in control group. Data on demographic features (age, gender, family history of atopy) and laboratory values of serum eosinophil, total IgE, IgM, IgA, IgG levels and skin prick test results were collected through patient files. The disease severity was assessed by SCORAD index. IL-31 levels were measured with human IL-31 ELISA kit. Results: The statistical analysis showed that IL-31 level was significantly higher in AD patients than in the control group (AD vs CG, p 0.0001). There was no significant difference in IL-31 levels between the three subgroups divided according to the SCORAD severity score (p:0.27). Conclusion: IL-31 levels were significantly higher in AD patients compared to control group but irrelevant to the disease severity


No disponible


Assuntos
Humanos , Masculino , Feminino , Pré-Escolar , Criança , Dermatite Atópica/imunologia , Interleucinas/imunologia , Dermatite Atópica/complicações , Interleucinas/sangue , Prurido/sangue , Prurido/etiologia , Índice de Gravidade de Doença
3.
Nutr. hosp ; 35(4): 957-961, jul.-ago. 2018. tab, graf
Artigo em Espanhol | IBECS | ID: ibc-179892

RESUMO

Introducción: la alteración histológica en el intestino delgado de los enfermos celiacos produce una pobre absorción que deteriora o dificulta una ganancia óptima de peso. Esto puede ser el resultado de un aumento de la expresión de las interleuquinas Th17 gluten-específicas. Objetivo: el objetivo de este estudio fue comparar la expresión de las interleuquinas Th17 en pacientes celiacos con peso normal y sobrepeso/ obesidad. Métodos: se estudiaron 22 pacientes con reciente diagnóstico de enfermedad celiaca: 15 con peso normal y siete con sobrepeso/obesidad. Se tomaron biopsias de intestino delgado para la evaluación de la expresión de las interleuquinas a través de PCR a tiempo-real. Resultados: los niveles de expresión de las interleuquinas Th17 mostraron una tendencia a ser más altos en las biopsias de intestino de pacientes con sobrepeso/obesidad en comparación a los celiacos con peso normal, sin embargo, esta diferencia no fue significativa. Conclusión: el exceso de peso en pacientes celiacos no es influenciado por los niveles de expresión de interleuquinas Th17


Introduction: the histological alteration in the small intestine of the celiac patients produces a poor absorption that deteriorates or hinder an optimal weight gain. This can be the result of an increase expression of the Th17 gluten-specific interleukins. Objective: the aim of this study was to compare the expression of Th17 interleukins in celiac patients with normal and overweight/obese nutritional status. Methods: a total of 22 patients with newly diagnosed celiac disease were eligible: 15 patients with normal weight and seven overweight/obese. Small intestine biopsies were taken for the evaluation of the expression of interleukins through real-time PCR. Results: expression levels of Th17 interleukins showed a tendency to be higher in intestinal biopsies of overweight/obese patients compared to normal weight celiac subjects; however, this difference was not statistical significant. Conclusion: body weight excess in celiac patients is not influenced by the expression levels of Th17 interleukins


Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Doença Celíaca/complicações , Doença Celíaca/genética , Interleucinas/genética , Interleucinas/metabolismo , Obesidade/genética , Sobrepeso/genética , Células Th17/metabolismo , Doença Celíaca/patologia , Intestino Delgado/patologia , Estado Nutricional , Obesidade/etiologia , Sobrepeso/etiologia
4.
Angiol. (Barcelona) ; 70(2): 70-78, mar.-abr. 2018. graf, ilus
Artigo em Espanhol | IBECS | ID: ibc-172329

RESUMO

La sepsis es una enfermedad de origen infeccioso con una prevalencia de 2.911 por 100.000 pacientes en Estados Unidos, y se caracteriza por el desbalance de la respuesta pro y antiinflamatoria por parte del sistema inmune. Sin embargo, la falta de comprensión de la respuesta del huésped frente a la infección justifica la importancia de su debate. En esta revisión no sistemática se plantea la relación funcional que existiría entre el receptor de adenosina A2A (A2A), óxido nítrico (NO) y factor de crecimiento vascular (VEGF), los cuales regulan la vasodilatación y la permeabilidad microvascular, y que en la sepsis se encuentran alterados. La evidencia revisada muestra que en el medio extracelular expuesto a infección se genera un estado de hipoxia celular, la que aumenta la producción de adenosina, nucleósido derivado del metabolismo del ATP. Esta molécula, al activar el receptor A2A presente en células del sistema inmune y endoteliales es capaz de reducir la respuesta inmunológica y aumentar la permeabilidad vascular, lo que a su vez ha sido asociado con una mayor progresión bacteriana y fallo multisistémico. Molecularmente, A2A activa la síntesis y producción de NO y VEGF. Por su parte, VEGF, al activar su receptor tipo 2 aumenta también la producción de NO, generando un circulo potenciador del efecto inmunológico y vascular. Pese a estas evidencias no hemos encontrado estudios que relacionen directamente estos 3 actores, A2A-NO y VEGF en la sepsis. Por ello, a la luz de la evidencia revisada, proponemos que la vía A2A-NO-VEGF sería un blanco de estudio en la fisiopatología y tratamiento de la sepsis (AU)


Sepsis is an infectious disease with a prevalence of 2.9 per 100 individuals in the United States. It is characterised by an unbalanced pro- and anti-inflammatory response driven by the immune system. However, further discussion is needed due to the lack of understanding on the details of the host response to the infection. This non-systemic review addresses the functional relationship between the Adenosine 2A receptor (A2A), Nitric Oxide (NO), and Vascular Epithelial Growth Factor (VEGF), which regulate vasodilation and micro-vascular permeability, which in turn are affected in sepsis. The evidence reviewed shows that an state of cellular hypoxia is generated due to infection, which increases the production of adenosine (ADO), a nucleoside derived from the metabolism of ATP. This molecule, by activating A2A receptor present in cells of the immune and endothelial systems reduces the immune response and increasing vascular permeability, which in turn has been associated with greater bacterial progression and multisystem failure. Molecularly, A2A activates the synthesis and production of NO and VEGF. In this regard, VEGF, by activating its type 2 receptor (VEGFR2) also increases NO production. This generates a cycle that enhances the immunological and vascular effect. Despite this, no studies were found that directly links these three actors, A2A-NO and VEGF, in sepsis. Therefore, taking into account the reviewed evidence, it is proposed that the A2A-NO-VEGF pathway could be a target of study in the pathophysiology and treatment of sepsis (AU)


Assuntos
Humanos , Animais , Agonistas do Receptor A2 de Adenosina/uso terapêutico , Óxido Nítrico/uso terapêutico , Endotélio Vascular/cirurgia , Sepse/enzimologia , Sepse/cirurgia , Interleucinas/uso terapêutico , Sepse/fisiopatologia , Imunossupressão/métodos
5.
J. physiol. biochem ; 73(4): 523-530, nov. 2017. tab
Artigo em Inglês | IBECS | ID: ibc-178902

RESUMO

Exercise intensity usually correlates with increased oxidative stress and enhanced cytokine production. However, it is unknown if all types of exercise that induce muscle damage can cause a parallel response in the oxidation balance and cytokine production. To this end, the effect of a 2000-m running test in a group of volunteers that regularly train in aerobic routines was studied. Different circulating parameters were measured, oxidative stress markers (protein carbonyls and malondialdehyde), antioxidant enzyme activity, and cytokine levels in plasma as well as in the main circulating cells of blood samples obtained in basal conditions and after test execution. As a result, the test caused muscle damage evidenced by an increase in circulating creatine kinase and myoglobin. This was accompanied by an increase in protein carbonyls in plasma and peripheral blood mononuclear cells. Activities of antioxidant enzymes (catalase, glutathione peroxidase and reductase, superoxide dismutase) were elevated in peripheral blood mononuclear cells, neutrophils, and erythrocytes after the test. Regarding cytokine production, interleukin-6, interleukin-8, interleukin-10, and tumor necrosis factor-α exhibited no significant changes after the test. Results suggest that this short but intense running exercise (2000 m) can induce muscle damage and elicit a good balance between oxidant/antioxidant responses with no changes in the circulating concentration of pro-inflammatory cytokines


No disponible


Assuntos
Humanos , Masculino , Antioxidantes/metabolismo , Citocinas/sangue , Corrida , Inflamação , Interleucinas
6.
Endocrinol. diabetes nutr. (Ed. impr.) ; 64(6): 317-327, jun.-jul. 2017. ilus
Artigo em Espanhol | IBECS | ID: ibc-171728

RESUMO

La inflamación generada en el tejido adiposo o lipoinflamación, puede contribuir al desarrollo de la resistencia a la insulina. Los mecanismos asociados a la lipoinflamación están relacionados con la función de los adipocitos y los macrófagos presentes en el tejido adiposo. En este contexto, el nivel del nucleósido adenosina está aumentado en individuos con obesidad. Las causas o consecuencias de este aumento no se conocen. Aunque, adenosina al activar a sus receptores (A1, A2A, A2B y A3) es capaz de modular diferencialmente la función de adipocitos y macrófagos, con el fin de evitar la reducción de la sensibilidad a la insulina y generar un estado antiinflamatorio en el individuo con obesidad. En esta revisión proponemos que adenosina podría ser un elemento clave en el desarrollo de nuevas estrategias para el control de la lipoinflamación y homeostasis metabólica a través de la regulación del diálogo adipocito-macrófago (AU)


Lipoinflamation is the inflammation generated in the adipose tissue. It can contribute to the development of insulin resistance. The lipoinflammation-associated mechanisms are related to the function of adipocytes and macrophages present in the adipose tissue. In this regard, the level of nucleoside adenosine is increased in individuals with obesity. Causes or consequences of this increase are unknown. Although, adenosine activating its receptors (A1, A2A, A2B and A3) is able to differentially modulate the function of adipocytes and macrophages, in order to avoid the reduction of insulin sensitivity and generate an anti-inflammatory state in subject with obesity. In this review we propose that adenosine could be a key element in the development of new strategies for limit lipoinflammation and regulate metabolic homeostasis through modulation of adipocyte-macrophage dialogue (AU)


Assuntos
Humanos , Adenosina/metabolismo , Adipócitos/metabolismo , Obesidade/diagnóstico , Interleucinas/análise , Receptor A2A de Adenosina/análise , Macrófagos , Receptor A2B de Adenosina/análise , Tecido Adiposo , Obesidade/complicações
9.
J. physiol. biochem ; 71(2): 191-204, jun. 2015.
Artigo em Inglês | IBECS | ID: ibc-140528

RESUMO

Breast cancer is the most prevalent malignant neoplasm in the world, and chemoprevention through dietary intervention strategy is an emerging option to reduce the incidence. D-pinitol (DP), a major component of soya bean, possesses attractive biological actions. We have investigated whether D-pinitol have an effect on tumor growth in vivo against 7,12-dimethylbenz(a)anthracene (DMBA)-initiated rat mammary carcinogenesis and investigated its mechanism of action. Tumors were induced in Sprague–Dawley (SD) rats by a gastric dose of 20 mg/kg DMBA, and after 13 weeks of induction period, the rats were orally administered with D-pinitol for 45 days. At the end of the assay, animals in carcinogen control group prompted a tumor incidence of 100 % and developed a tumor volume of 8.35 ± 0.56, which was significantly reduced to 5.74 ± 0.32 for the animals treated with D-pinitol. The D-pinitol treatment not only decreased the tumor volume but also further examination revealed that tumors from animals that received D-pinitol reduced nuclear factor kappa B (NF-κB) activation which in turn results in modulation of its downstreaming p53 and proteins of caspase-3 family. Bcl-2 expression and caspase-3 activation were also decreased after D-pinitol supplementation leading to induction of apoptosis and finally cell death. Furthermore, the status of the inflammatory cytokines such as tumor necrosis factor-alfa (TNF-alfa), interleukin (IL)-2, IL-6, and tumor markers, lipid profile, and hormones was also significantly declined up on D-pinitol administration. Thus, it reveals the collective involvement of the abovementioned parameters along with NF-κB signaling through which D-pinitol induces apoptosis and subsequently suppresses breast cancer during DMBA-induced rat breast carcinogenesis (AU)


No disponible


Assuntos
Animais , Ratos , Soja , Compostos Fitoquímicos/farmacocinética , Neoplasias da Mama/prevenção & controle , NF-kappa B/antagonistas & inibidores , Substâncias Protetoras/farmacocinética , Interleucinas , Apoptose , Carcinogênese
10.
Allergol. immunopatol ; 42(6): 603-608, nov.-dic. 2014. tab
Artigo em Inglês | IBECS | ID: ibc-130152

RESUMO

Asthma is a complex disease involving numerous mediator molecules and effector cells, in combination with a range of environmental determining factors. Cytokines play a key role in the physiopathological mechanisms of asthma; the study of the structure, regulation and variations of the genes that encode for these molecules is therefore crucial. Cytokines have extremely diverse roles, and exert effects both as activators and inhibitors of the innate and adaptive immune response. Certain modifications in the expression or structure of these molecules, resulting from the presence of polymorphisms, may give rise to deregulation of the mentioned effects, and therefore to a predisposition to develop concrete asthma phenotypes (AU)


No disponible


Assuntos
Humanos , Citocinas/análise , Asma/fisiopatologia , Hipersensibilidade Respiratória/fisiopatologia , Inflamação/fisiopatologia , Interleucinas/análise , Fatores de Crescimento Transformadores/análise , Linfotoxina-alfa/análise
11.
Allergol. immunopatol ; 42(5): 402-406, sept.-oct. 2014. tab, graf
Artigo em Inglês | IBECS | ID: ibc-127272

RESUMO

Background: Although some studies show that IL-22 and IL-25 play critical roles in the pathogenesis of asthma, little is known about the systemic production of these cytokines. The aim of this study was to assay IL-22 and IL-25 in serum, in mitogen-activated whole blood (WB), and in mitogen-activated peripheral blood mononuclear cell (PBMC) cultures of patients with severe asthma. Methods: In this cross-sectional study, a questionnaire was prepared to determine the severity of asthma. Through the questionnaire, information including clinical signs, clinical symptoms, and past medical history were acquired. Information collected allowed all patients who were active or ex-smokers to be excluded. A trained observer assessed airway reversibility, peak flowmetry, and spirometry in the remaining patients. Twenty-one patients and simultaneously, twenty age- and sex-matched healthy controls were selected. Sterile blood (10 ml) was taken from each study participant. Sera were isolated and anticoagulant blood used for WB and PBMC cultures and haematological tests. Phytohaemagglutinin and lipopolysaccharide (LPS) were used to activate WB and PBMC. The data from these two groups were compared using Student's t-test. Results: Although the total white blood cell count was elevated in the asthmatic group, other haematological indices, including IL-22 and IL-25 levels in the asthmatic group were not significantly (p > 0.05) different from controls. Conclusions: The levels of IL-22 and IL-25 in patients with severe asthma are no higher than those of non-asthmatic individuals. Any major role for IL-22 and IL-25 in severe asthma is likely to be localised to the lungs and bronchial tissues (AU)


No disponible


Assuntos
Humanos , Masculino , Feminino , Asma/sangue , Asma/imunologia , Asma/prevenção & controle , Testes Hematológicos/tendências , Sangue/imunologia , Análise Química do Sangue/métodos , Análise Química do Sangue/tendências , Interleucinas/imunologia , Estudos de Casos e Controles
12.
Allergol. immunopatol ; 42(5): 465-471, sept.-oct. 2014. graf, tab
Artigo em Inglês | IBECS | ID: ibc-127282

RESUMO

Background: This study was performed to investigate the serum level of interleukin (IL)-13, IL-4, and interferon (IFN)-γ in chronic rhinosinusitis with nasal polyps (CRSwNP) and subsequent inflammation pattern and comorbidities including asthma and aspirin intolerance. Methods: A case-control study was conducted on 60 adult patients with CRSwNP with mean age of 37.7 ± 12.7 (ranging from 18 to 70) years, and on 20 healthy controls. Serum levels of IL-13, IL-4, and IFN-γ were assessed, using enzyme-linked immunosorbent assay to be compared between case and control groups. Serum level of total immunoglobulin (Ig) E was also assessed in the patients with CRSwNP. Results: Serum level of IL-13 in the patients with CRSwNP was significantly higher than the controls (0.98 ± 1.56 vs. 0.34 ± 0.16 pg/ml, respectively, p = 0.002). IL-4 and IFN-γ did not differ significantly between the two groups. Total IgE level was significantly increased in the patients with CRSwNP, compared to the normal values (301.43 ± 516.54 IU/ml, p = 0.033). Among the patients with CRSwNP, 12/60 (20%) had aspirin intolerance and 44/60 (73.3%) had asthma. IgE was also higher in asthmatics than non-asthmatics patients (364.9 ± 586.6 vs. 126.7 ± 135.7, respectively, p = 0.015). Patients with aspirin intolerance had higher levels of IFN-γ (4.7 ± 1.4 vs. 4.1 ± 0.6, respectively, p = 0.022). Conclusions: IL-13 with high level of total IgE was observed in the patients with CRSwNP, which predisposes them to have concomitant asthma. IFN-γ seems to be down-regulated in the patients with CRSwNP, but could be over-expressed in the presence of aspirin intolerance (AU)


No disponible


Assuntos
Humanos , Masculino , Feminino , Adulto Jovem , Adulto , Pessoa de Meia-Idade , Idoso , Sinusite/diagnóstico , Sinusite/imunologia , Pólipos Nasais/imunologia , Pólipos Nasais/fisiopatologia , Asma/imunologia , Interleucinas , Interleucinas/imunologia , Imunoglobulina E/imunologia , Estudos de Casos e Controles , Medidas de Volume Pulmonar , Análise Química do Sangue/tendências
14.
Nutr. hosp ; 29(2): 259-268, 2014. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-120583

RESUMO

Introducción: Los diferentes tipos de cáncer constituyen una de las principales causas de morbi-mortalidad en el mundo. La terapia clásica antitumoral (cirugía, quimioterapia, radioterapia) ha incrementado notoriamente la supervivencia. Las terapias biológicas, con mecanismos de acción selectivos y frecuentemente específicos, constituyen una incorporación relativamente reciente al tratamiento oncológico; entre las más utilizadas se incluyen: citoquinas, anticuerpos monoclonales e inhibidores de tirosin kinasa y de mTOR. Si bien están adecuadamente documentados los efectos adversos nutricionales y metabólicos asociados a la terapia clásica, tanto en literatura como en guías clínicas, no ocurre igual con la terapia biológica. Objetivo: Revisar la literatura al respecto y detallar de modo organizado los resultados obtenidos. Métodos: Se revisó la literatura indizada así como todas las fichas técnicas de los fármacos incluidos en las distintas familias mediante la Agencia Española del Medicamento y Productos Sanitarios a Julio de 2013. Se registran los síntomas y signos clínicos con teórica acción sobre el estado nutricional o metabólico. Resultados: Se describe la acción específica de cada familia. Se agrupan los posibles efectos adversos de cada una sobre el estado nutricional y metabolismo, detallando y diferenciándolos en tablas para una más fácil y cómoda revisión y consulta. Se observan como posibles efectos secundarios más prevalentes los relacionados con el apetito, aparato digestivo y alteraciones electrolíticas. Conclusiones: Los posibles efectos secundarios asociados a terapias biológicas son múltiples y aparecen con diferente frecuencia y gravedad. Es importante al utilizarlas conocer el impacto nutricional y metabólico que pueden presentar, para su prevención y tratamiento (AU)


Introduction: The different types of cancer represent one of the main causes of morbimortality worldwide. Classical anti-tumor therapy (surgery, chemotherapy, radiotherapy) has notably increased the survival rate. Biological therapies, with selective and frequently specific mechanisms of action, are a relatively recent acquisition in oncologic therapy; among the most commonly used ones are: cytokines, monoclonal antibodies, tyrosine kinase inhibitors, and mTOR inhibitors. The nutritional and metabolic adverse effects of classical therapy are well documented in the literature and the clinical guidelines, which is not the case for biological therapy. Objective: To review the literature in this field and to detail in an organized manner the results obtained. Methods: Indexed literature and the technical data sheets of the drugs included in the different families were revised through the Spanish Agency of Medicines and Health Care Products until July of 2013. The symptoms and clinical signs of a theoretical action on the nutritional and metabolic status were recorded. Results: The specific action of each family is described. The possible adverse effects of each one of them on the nutritional and metabolic status are grouped, detailing and differentiating them in tables for easier and more friendly-user consultation. The most prevalent possible side effects observed are those related with the appetite, the gastrointestinal tract, and electrolytic impairments. Conclusions: the possible side effects associated to biological therapies are plenty and occur with different frequency and severity. It is important to know the nutritional and metabolic impact when using these therapies for preventing and managing them (AU)


Assuntos
Humanos , Terapia Biológica/efeitos adversos , Desnutrição/etiologia , Neoplasias/complicações , Avaliação Nutricional , Transtornos Nutricionais/etiologia , Anticorpos Monoclonais/efeitos adversos , Interleucinas/efeitos adversos , Interferons/efeitos adversos , /efeitos adversos
15.
Rev. iberoam. micol ; 30(4): 217-225, oct.-dic. 2013.
Artigo em Espanhol | IBECS | ID: ibc-116764

RESUMO

El hierro es un elemento esencial para el crecimiento y la virulencia de la mayoría de los microorganismos. Dentro de los mecanismos de inmunidad innata (o nutricional) los mamíferos han desarrollado diversas estrategias para su transporte y almacenamiento, limitando así la disponibilidad de hierro libre en el medio. Para poder sobrevivir en este entorno hostil los hongos potencialmente patógenos disponen de mecanismos específicos para la captación del hierro, entre los que destaca la síntesis de sideróforos, moléculas solubles de bajo peso molecular con elevada capacidad de quelación. La sobrecarga férrica y el consiguiente aumento de la concentración de hierro libre son factores de riesgo para el desarrollo de infección fúngica invasiva (IFI) por Mucorales y Aspergillus. Por tanto, la reducción del hierro libre circulante mediante el uso de quelantes constituye un abordaje terapéutico atractivo. El primer quelante del hierro autorizado (deferoxamina) se reveló, paradójicamente, como un factor de riesgo para el desarrollo de IFI al actuar como un xenosideróforo para los Mucorales. Por el contrario, los quelantes orales de nueva generación (deferiprona y deferasirox) han demostrado inhibir el crecimiento fúngico in vitro y en modelos animales. La presente revisión analiza el papel del metabolismo férrico en la patogenia de la IFI, así como los datos preclínicos disponibles y la, hasta la fecha, limitada experiencia clínica que respalda el empleo de los nuevos quelantes del hierro en el tratamiento de la mucormicosis y de la aspergilosis invasiva (AU)


Assuntos
Micoses/complicações , Micoses/epidemiologia , Micoses/prevenção & controle , Mucormicose/complicações , Mucormicose/diagnóstico , Mucormicose/microbiologia , Aspergilose/epidemiologia , Aspergilose/prevenção & controle , Quelantes de Ferro/isolamento & purificação , Fatores de Risco , Interleucinas , Interleucinas/isolamento & purificação , Corticosteroides/uso terapêutico
16.
J. investig. allergol. clin. immunol ; 23(6): 428-434, sept.-oct. 2013. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-117652

RESUMO

Background: Interleukin (IL) 33, a novel member of the IL-1 family, is produced mainly by epithelial cells and endothelial cells in response to various types of stress, including necrosis. The effects of IL-33 on the immune cells involved in allergic contact dermatitis have recently been revealed in vitro. However, in vivo, the induction mechanism and function of IL-33 are not fully understood. Objectives: Our objectives were to investigate induction of IL-33 in keratinocytes and to evaluate the functions of IL-33 and its inducers in a murine model of allergic contact dermatitis. Material and Methods: KERTr cells, a human keratinocyte cell line, were cultured with various cytokines, including tumor necrosis factor (TNF) α and interferon (IFN) ƴ. IL-33 expression was detected using quantitative reverse transcriptase polymerase chain reaction, immunocytochemistry, and Western blotting. The functions of IL-33, TNF- α, and IFN-􀁡 in allergic contact dermatitis were evaluated using a murine model. Results: TNF- α and IFN- ƴ induced expression of IL-33 mRNA and protein in KERTr cells. Blockade of IL-33 attenuated swelling in the ears of the experimental mice. Similar effects were noted for blockade of TNF- α and IFN- ƴ in these mice. Conclusions: TNF- α and IFN- ƴ induce expression of IL-33, and IL-33 produced by keratinocytes contributes to allergic contact dermatitis. Blockade of IL-33, TNF- α, and IFN- ƴ could represent novel and potent strategies to treat allergic contact dermatitis (AU)


Antecedentes: La Interleucina 33 (IL-33), un nuevo miembro de la familia de la IL-1, es producida fundamentalmente por las células epiteliales y endoteliales en respuesta a diferentes estímulos, incluyendo la necrosis. Recientemente se han confirmado los efectos de esta IL sobre las células del sistema inmunológico in vitro en pacientes con dermatitis de contacto, aunque los mecanismos y función in vivo de la IL-33 no son bien conocidos. Objetivos: El objetivo de este estudio fue analizar los factores que podrían inducir IL-33 en queratinocitos y evaluar las funciones de esta citocina y de sus inductores en un modelo murino de dermatitis alérgica de contacto. Métodos: Para ello se cultivaron células KERTr, una línea celular de queratinocitos humanos, en presencia de varias citocinas, incluyendo TNF- α e IFN − ƴ. La expresión de IL-13 se detectó mediante PCR cuantitativa a tiempo real, inmunocitoquímica e inmunobloting. Así mismo se evaluó la función de IL-33, TNF- α, e IFN- ƴ en el modelo murino. Resultados: En cuanto a los resultados obtenidos TNF- α y IFN- ƴ indujeron la expresión de mRNA y expresión de proteína en las células KERTr. El bloqueo de IL-33 atenúa la inflación en la dermatitis de contacto murina. Efectos similares se obtienen mediante el bloqueo de TNF- α y IFN- ƴ. Conclusiones: En conclusión, TNF- α and IFN- ƴ son inductores de la producción de IL-33, y además esta citocina producida por los queratinocitos contribuye a la expresión de dermatitis alérgica de contacto. El bloqueo de no solo IL-33, sino también de TNF- α y IFN- ƴ podría representar una modalidad terapéutica nueva y potente en la dermatitis alérgica de contacto (AU)


Assuntos
Humanos , Fator de Necrose Tumoral alfa/imunologia , Dermatite Alérgica de Contato/imunologia , Interleucinas/imunologia , Interferons/imunologia , Queratinócitos/imunologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa/métodos , Imuno-Histoquímica/métodos
17.
Arch. bronconeumol. (Ed. impr.) ; 49(9): 383-387, sept. 2013. tab
Artigo em Espanhol | IBECS | ID: ibc-116679

RESUMO

Introducción: La anemia es una de las manifestaciones extrapulmonares de la enfermedad pulmonar obstructiva crónica (EPOC). Su prevalencia, su fisiopatología y su repercusión clínica son desconocidas. Los objetivos de nuestro estudio son determinar la prevalencia de la anemia en pacientes con EPOC en fase estable no atribuible a otras causas y establecer la relación de la anemia con variables clínicas, pronósticas y marcadores inflamatorios con un papel relevante en la EPOC. Métodos: Se incluyeron pacientes con EPOC en fase estable sin otras causas conocidas de anemia. Se realizaron pruebas de función respiratoria, determinación de eritropoyetina y marcadores inflamatorios séricos: PCR ultrasensible (PCR), fibrinógeno, interleucina 6 (IL-6), interleucina 8 (IL-8) y factor de necrosis tumoral alfa (TNF-α). Se registró el índice de masa corporal (IMC), el índice de Charlson y el BODE, el número de exacerbaciones en el año previo, la escala de disnea y la calidad de vida. Resultados: Se incluyeron 130 pacientes. La prevalencia de anemia fue del 6,2%. El valor de hemoglobina en los pacientes con anemia fue de 11,9 ± 0,95 g/dl. Los pacientes con anemia tenían un IMC más bajo (p = 0,03), un índice de Charlson mayor (p = 0,002), niveles de eritropoyetina más elevados (p = 0,016), una tendencia a presentar niveles más bajos de FEV1% (p = 0,08) y valores significativamente más bajos de IL-6 (p = 0,003) cuando se comparan con los pacientes no anémicos. Conclusiones: En nuestra serie, la anemia asociada a la EPOC es menos prevalente de lo publicado hasta la actualidad y guarda relación con determinados factores clínicos y marcadores inflamatorios (AU)


Background: Anaemia is one of the extrapulmonary manifestations of chronic obstructive pulmonary disease (COPD). Its real prevalence, physiopathology and clinical repercussion are unknown. The objectives of our study were: to determine the prevalence of anaemia in patients with stable COPD not attributable to other causes and to establish the relationship of anaemia with clinical, prognostic and inflammatory markers with an important role in COPD. Methods: The study included stable COPD patients with no other known causes of anaemia. The following tests were carried out: respiratory function tests; serum determination of erythropoietin and inflammatory markers: high sensitivity C -reactive protein (hs-CRP), fibrinogen, interleukin 6 (IL-6), interleukin 8 (IL-8) and tumour necrosis factor α (TNF-α). Body mass index (BMI), Charlson and BODE indices, the number of exacerbations in the previous year, dyspnoea and quality of life were also calculated. Results: One hundred and thirty patients were included. Anaemia prevalence was 6.2%. Mean haemoglobin value in anaemic patients was 11.9 ± 0.95 g/dL. Patients with anaemia had a lower BMI (P=0.03), higher Charlson index (P=0.002), more elevated erythropoietin levels (P=.016), a tendency to present a lower FEV1% value (P=.08) and significantly lower IL-6 values when compared to non-anaemic patients (P=0.003). Conclusions: In our series, the anaemia associated with COPD was less prevalent than that published in the literature to date, and was related to certain clinical and inflammatory markers (AU)


Assuntos
Humanos , Anemia/epidemiologia , Doença Pulmonar Obstrutiva Crônica/complicações , Interleucinas/análise , Biomarcadores/análise , Dispneia/epidemiologia , Qualidade de Vida
18.
Rev. esp. enferm. dig ; 105(7): 392-399, ago. 2013. tab, ilus
Artigo em Espanhol | IBECS | ID: ibc-116834

RESUMO

Antecedentes: evidencias recientes han mostrado una alteración en la regulación inmune en el síndrome de intestino irritable (SII) así como variaciones en los polimorfismos de citocinas. Objetivos: determinar la frecuencia de polimorfismos IL-10 (-1082G/A) y TNF-alpha (-308G/A) en sujetos con SII en México. Métodos: sujetos voluntarios contestaron el Cuestionario de Roma II y fueron clasificados como SII (n = 45) y controles (n = 92). Aquellos con SII fueron a su vez clasificados en SII-D: 22,2 %, SII-E: 28,9 % y SII-A/M: 48,9 %. Se comparó la frecuencia de los polimorfismos entre los grupos. Resultados: no hubo diferencias entre SII vs. controles en la frecuencia del genotipo alto (8,9 vs. 18,5 %), intermedio (60,0 vs. 57,6 %) y bajo productor (23,9 vs. 38,9 %) de IL-10, p = 0,315. Tampoco en alto (0 vs. 1,1 %), intermedio (55,4 vs. 43,2 %) o bajo productor (43,5 vs. 56,8 %) de TNF-alpha, p = 0,296. Sin embargo, el bajo productor de IL-10 fue más frecuente en SII-D vs. SII-E vs. SII-A/M (63,6 vs. 7,1 vs. 33,3 %) p = 0,023. Conclusiones: en este grupo de voluntarios en México la frecuencia de genotipos de IL-10 (-1082G/A) y TNF-alpha (-308G/A) fue similar en SII y controles, pero aquellos con SII-D presentaron mayor frecuencia del bajo productor de IL-10 sugiriendo una predisposición genética a una regulación inmune anormal dada por un menor componente antiinflamatorio en este subgrupo (AU)


Background: there has been recent evidence of an alteration in irritable bowel syndrome (IBS) immune regulation, as well as variations in cytokine polymorphisms. Aims: to determine the frequency of the IL-10 (-1082G/A) and TNF-áalpha(-308G/A) polymorphisms in subjects with IBS in Mexico. Methods: volunteers answered the Rome II Questionnaire and were classified as IBS (n = 45) and controls (n = 92). The IBS subjects were then categorized as IBS-D: 22.2 %, IBS-C: 28.9 %, and IBS-A/M: 48.9 %. The polymorphism frequency among groups was compared. Results: there were no differences between IBS vs. controls in the frequency of the high (8.9 vs. 18.5 %), intermediate (60.0 vs. 57.6 %), or low (23.9 vs. 38.9 %) producer IL-10 genotypes, p = 0.315. Neither were there differences in the high (0 vs. 1.1 %), intermediate (55.4 vs. 43.2 %), or low (43.5 vs. 56.8 %) producer TNF-alpha genotypes, p = 0.296. However the low producer of IL-10 was more frequent in IBS-D vs. IBS-C vs. IBS-A/M (63.6 vs. 7.1 vs. 33,3 %) p = 0.023. Conclusions: in this group of volunteers in Mexico, the frequency of the IL-10 (-1082G/A) and TNF-alpha (-308G/A) genotypes was similar in IBS and controls. However, there was a greater frequency of the low producer of IL-10 in those subjects with IBS-D, suggesting a genetic predisposition to abnormal immune regulation due to a lower anti-inflammatory component in this subgroup (AU)


Assuntos
Humanos , Masculino , Feminino , Fator de Necrose Tumoral alfa , Fator de Necrose Tumoral alfa/metabolismo , Síndrome do Intestino Irritável/complicações , Síndrome do Intestino Irritável/diagnóstico , Polimorfismo Genético/genética , Genótipo , Interleucinas , Receptores de Interleucina , Anti-Inflamatórios não Esteroides/uso terapêutico , Síndrome do Intestino Irritável/epidemiologia , Síndrome do Intestino Irritável/fisiopatologia , Síndrome do Intestino Irritável/terapia , Inquéritos e Questionários , Constipação Intestinal/epidemiologia
19.
Reumatol. clín. (Barc.) ; 9(2): 106-112, mar.-abr. 2013. ilus, tab
Artigo em Espanhol | IBECS | ID: ibc-110342

RESUMO

La artritis reumatoide (AR) es una enfermedad sistémica e inflamatoria que afecta la membrana sinovial de las articulaciones, los tendones y algunos sitios extra-articulares. La prevalencia de la AR en Latinoamérica se encuentra entre 0.4–1.6%. El tratamiento precoz de la enfermedad se traduce en una reducción del costo para la sociedad. En vista de esto, se han establecido clínicas de AR temprana en varios países de la región. Se han identificado barreras para el tratamiento de la AR como lo son el retraso en la referencia al reumatólogo y limitaciones en el acceso al tratamiento. Varios países han desarrollado y adaptado guías para el tratamiento basadas en la evidencia y en sus propias realidades. La necesidad de tener registros detallados de las prescripciones de biológicos ha sido abordada con registros de biológicos lo que llevará a un mejor entendimiento de las enfermedades reumáticas y su tratamiento. Los biológicos disponibles en la actualidad son los inhibidores del factor de necrosis tumoral (TNF)-alpha (etanercept, infliximab y adalimumab), un agente depletor de células B (rituximab), un bloqueador del receptor de interleucina-6 (tocilizumab) y un bloqueador de la co-estimulación de células T (abatacept). En el futuro se incluirán los inhibidores de cinasas (tofacitinib y fostamatinib) e inhibidores del TNF-alpha alternativos (golimumab y certolizumab) y biosimilares (AU)


Rheumatoid arthritis (RA) is a systemic inflammatory disease affecting the synovium of joints, tendons, and some extra-articular sites. RA prevalence in Latin America ranges from 0.4 to 1.6%. Early treatment of RA translates into a substantial reduction in the cost to society. In light of this, early disease clinics are being established in some countries. Barriers to RA management, such as delay in referral to rheumatologists and limited access to therapy, have been identified. Evidence-based treatment guidelines have been adapted by countries according to their own situations. The need for keeping accurate records of biologics prescribed has been addressed by biologic registries, thereby contributing toward a better understanding of rheumatic diseases and their treatment. Current biologics include the tumor necrosis factor (TNF)-alpha inhibitors (etanercept, infliximab, and adalimumab), B-cell depletion agent (rituximab), interleukin-6 receptor blocker (tocilizumab), and T-cell co-stimulatory blocker (abatacept). Future therapies include kinase inhibitors (tofacitinib and fostamatinib), alternative TNF-alpha inhibitors (golimumab and certolizumab), and biosimilars (AU)


Assuntos
Humanos , Masculino , Feminino , Artrite Reumatoide/epidemiologia , Artrite Reumatoide/prevenção & controle , Diagnóstico Precoce , Interleucinas/uso terapêutico , Receptores de Interleucina/uso terapêutico , Fatores Socioeconômicos , América Latina/epidemiologia , Artrite Reumatoide/economia , Fator de Necrose Tumoral alfa/uso terapêutico , Receptores do Fator de Necrose Tumoral/uso terapêutico , Análise Socioeconômica
20.
Actas dermo-sifiliogr. (Ed. impr.) ; 103(10): 853-862, dic. 2012. graf, ilus
Artigo em Espanhol | IBECS | ID: ibc-107746

RESUMO

Uno de los aspectos clínicamente más relevantes de los recientes avances en el conocimiento de la psoriasis es su asociación con un aumento en la prevalencia de factores de riesgo cardiovascular, que determina un mayor riesgo de morbimortalidad relacionada con infarto agudo de miocardio, accidente cerebrovascular y arteriopatía periférica. La inflamación sistémica crónica asociada podría explicar en gran medida que la psoriasis moderada-grave sea un factor de riesgo independiente de enfermedad cardiovascular. La introducción de la terapia biológica ha mejorado en gran medida nuestras expectativas terapéuticas y el control a largo plazo de la enfermedad, y existen evidencias epidemiológicas de que puede mejorar también el riesgo cardiovascular, como ocurre en los pacientes con artritis reumatoide. Sin embargo, se han descrito algunos efectos adversos del tratamiento con agentes bloqueadores del factor de necrosis tumoral alfa en pacientes con insuficiencia cardíaca congestiva avanzada que obligan a tener especial precaución con su empleo en estos pacientes. Por otra parte, recientemente se ha observado un desequilibrio (aunque no estadísticamente significativo) en el número de acontecimientos adversos cardiovasculares mayores, que incluyen infarto de miocardio no letal, accidente cerebrovascular no letal y muertes de causa cardiovascular, en la fase controlada con placebo de los ensayos clínicos con briakinumab y ustekinumab, 2 anticuerpos monoclonales dirigidos contra p40, la subunidad común a IL-12 e IL-23. En el presente artículo se revisa la evidencia científica disponible en este campo (AU)


One of the most clinically important aspects of recent advances in our understanding of psoriasis has been the detection of an association between this disease and an increased prevalence of cardiovascular risk factors. This increase in prevalence is, in turn, linked to a greater risk of morbidity and mortality related to acute myocardial infarction, cerebrovascular accident, and peripheral arterial disease. The chronic systemic inflammation present in psoriasis could explain why moderate to severe psoriasis is an independent risk factor for cardiovascular disease. The introduction of biologic therapies has greatly improved the expectations of treatment as well as the long-term control of psoriasis, and there is epidemiological evidence that these therapies may lower cardiovascular risk in psoriasis as they do in rheumatoid arthritis. Caution should, however, be exercised when prescribing biologic drugs in this setting, because adverse effects have been reported in association with the use of tumor necrosis factor inhibitors in patients with advanced congestive heart failure. Furthermore, a numerical imbalance(without statistical significance) between the groups receiving the biologic drug and the placebo groups was recently observed in the incidence of major cardiovascular events (non fatal myocardial infarction and cerebrovascular accident and cardiovascular death) during the controlled periods of clinical trials of briakinumab and ustekinumab, 2 monoclonal antibodies that target the p40 subunit shared by IL 12 and IL-23. We review the current scientific evidence on this topic (AU)


Assuntos
Humanos , Psoríase/complicações , Doenças Cardiovasculares/epidemiologia , Terapia Biológica/métodos , Fatores de Risco , Anticorpos Monoclonais/uso terapêutico , Interleucinas/uso terapêutico
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