Your browser doesn't support javascript.
Mostrar: 20 | 50 | 100
Resultados 1 - 20 de 21
Filtrar
Mais filtros










Intervalo de ano de publicação
1.
Rev Esp Enferm Dig ; 1122019 Dec 13.
Artigo em Inglês | MEDLINE | ID: mdl-31830796

RESUMO

Celiac disease (CeD) and inflammatory bowel disease (IBD) are chronic gastrointestinal disorders of inflammatory origin that develop in response to environmental triggers in genetically predisposed individuals. CeD localizes in the duodenal mucosa, where intolerance develops to dietary gluten from wheat, barley, rye, and some varieties of oats. IBD, in turn, is subdivided primarily into Crohn's disease (CD) and colitis, with ulcerative colitis (UC) being the most thoroughly investigated form.

3.
Aliment Pharmacol Ther ; 49(12): 1484-1492, 2019 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-31074004

RESUMO

BACKGROUND: Treatment for coeliac disease is a lifelong strict gluten-free diet. Although guidelines recommend regular follow-up with dietary interviews and coeliac serology, these methods may be inaccurate. AIM: To evaluate the usefulness of faecal gluten immunogenic peptides to support the diagnosis and to determine the adherence to the gluten-free diet in coeliac children. METHODS: Multicentre prospective observational study including 64 coeliac children. Faecal gluten peptides, and tissue transglutaminase and deamidated gliadin peptide antibodies were analyzed at diagnosis, and 6, 12 and 24 months thereafter. Gluten consumption was estimated from gluten peptide levels. RESULTS: Most children (97%) had detectable gluten peptides at diagnosis. On a gluten-free diet, the rate of gluten peptides increased from 13% at 6 months to 25% at 24 months. Mean estimated gluten exposure dropped from 5543 mg/d at diagnosis to 144 mg/d at 6 months, then increased to 606 mg/d by 24 months. In contrast, deamidated gliadin peptide antibodies normalised and only 20% had elevated tissue transglutaminase antibody by 24 months. The elevation of tissue transglutaminase antibody was more prolonged in patients with detectable gluten peptides (P < 0.05). Nevertheless, absolute levels of tissue transglutaminase antibody had low sensitivity to identify patients with detectable gluten peptides (P > 0.1). Dietitian assessment was only moderately correlated with gluten peptide detection (κ = 0.5). CONCLUSIONS: Faecal gluten peptides testing may guide treatment of coeliac disease prior to diagnosis and during the assessment diet adherence. Further studies could determine if early identification of gluten exposure reduces the need for expensive/invasive investigations for non-responsive coeliac disease. ClinicalTrials.gov Number: NCT02711397.

6.
Rev Esp Enferm Dig ; 110(7): 458-461, 2018 07.
Artigo em Inglês | MEDLINE | ID: mdl-29722267

RESUMO

Coeliac disease (CD) is a chronic autoimmune enteropathy triggered by gluten and related prolamines in genetically predisposed individuals. Although CD is a polygenic disease, there is a strong association with genes of the human leukocyte antigen (HLA) region. Most patients present the HLA-DQ2 heterodimer, specifically the DQ2.5 isoform, which is present in around 90-96% of patients of European ancestry.


Assuntos
Doença Celíaca/diagnóstico , Doença Celíaca/genética , Antígenos HLA/genética , Predisposição Genética para Doença , Humanos
7.
Gut Microbes ; 9(6): 551-558, 2018 11 02.
Artigo em Inglês | MEDLINE | ID: mdl-29672211

RESUMO

Celiac disease (CD) is an immune-mediated enteropathy involving genetic and environmental factors, whose interaction influences disease risk. The intestinal microbiota, including viruses and bacteria, could play a role in the pathological process leading to gluten intolerance. In this study, we investigated the prevalence of pathogens in the intestinal microbiota of infants at familial risk of developing CD. We included 127 full-term newborns with at least one first-degree relative with CD. Infants were classified according to milk-feeding practice (breastfeeding or formula feeding) and HLA-DQ genotype (low, intermediate or high genetic risk). The prevalence of pathogenic bacteria and viruses was assessed in the faeces of the infants at 7 days, 1 month and 4 months of age. The prevalence of Clostridium perfringens was higher in formula-fed infants than in breast-fed over the study period, and that of C. difficile at 4 months. Among breastfed infants, a higher prevalence of enterotoxigenic E. coli (ETEC) was found in infants with the highest genetic risk compared either to those with a low or intermediate risk. Among formula-fed infants, a higher prevalence of ETEC was also found in infants with a high genetic risk compared to those of intermediate risk. Our results show that specific factors, such as formula feeding and the HLA-DQ2 genotype, previously linked to a higher risk of developing CD, influence the presence of pathogenic bacteria differently in the intestinal microbiota in early life. Further studies are warranted to establish whether these associations are related to CD onset later in life.


Assuntos
Bactérias/isolamento & purificação , Doença Celíaca/microbiologia , Microbioma Gastrointestinal , Predisposição Genética para Doença , Bactérias/classificação , Bactérias/genética , Doença Celíaca/genética , Clostridium/isolamento & purificação , Escherichia coli Enterotoxigênica/isolamento & purificação , Fezes/microbiologia , Fezes/virologia , Comportamento Alimentar , Microbioma Gastrointestinal/genética , Genótipo , Antígenos HLA-DQ/genética , Humanos , Recém-Nascido , Risco , Espanha
9.
Am J Gastroenterol ; 111(10): 1456-1465, 2016 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-27644734

RESUMO

OBJECTIVES: Treatment for celiac disease (CD) is a lifelong strict gluten-free diet (GFD). Patients should be followed-up with dietary interviews and serology as CD markers to ensure adherence to the diet. However, none of these methods offer an accurate measure of dietary compliance. Our aim was to evaluate the measurement of gluten immunogenic peptides (GIP) in stools as a marker of GFD adherence in CD patients and compare it with traditional methods of GFD monitoring. METHODS: We performed a prospective, nonrandomized, multicenter study including 188 CD patients on GFD and 84 healthy controls. Subjects were given a dietary questionnaire and fecal GIP quantified by enzyme-linked immunosorbent assay (ELISA). Serological anti-tissue transglutaminase (anti-tTG) IgA and anti-deamidated gliadin peptide (anti-DGP) IgA antibodies were measured simultaneously. RESULTS: Of the 188 celiac patients, 56 (29.8%) had detectable GIP levels in stools. There was significant association between age and GIP in stools that revealed increasing dietary transgressions with advancing age (39.2% in subjects ≥13 years old) and with gender in certain age groups (60% in men ≥13 years old). No association was found between fecal GIP and dietary questionnaire or anti-tTG antibodies. However, association was detected between GIP and anti-DGP antibodies, although 46 of the 53 GIP stool-positive patients were negative for anti-DGP. CONCLUSIONS: Detection of gluten peptides in stools reveals limitations of traditional methods for monitoring GFD in celiac patients. The GIP ELISA enables direct and quantitative assessment of gluten exposure early after ingestion and could aid in the diagnosis and clinical management of nonresponsive CD and refractory CD. Trial registration number NCT02711397.


Assuntos
Autoanticorpos/imunologia , Doença Celíaca/dietoterapia , Registros de Dieta , Dieta Livre de Glúten , Fezes/química , Proteínas de Ligação ao GTP/imunologia , Gliadina/imunologia , Glutens/análise , Imunoglobulina A/imunologia , Cooperação do Paciente , Transglutaminases/imunologia , Adolescente , Fatores Etários , Anticorpos/imunologia , Estudos de Casos e Controles , Doença Celíaca/imunologia , Criança , Pré-Escolar , Ensaio de Imunoadsorção Enzimática , Feminino , Humanos , Lactente , Masculino , Estudos Prospectivos , Testes Sorológicos , Inquéritos e Questionários , Adulto Jovem
10.
Rev Esp Enferm Dig ; 106(5): 334-45, 2014 May.
Artigo em Inglês | MEDLINE | ID: mdl-25287236

RESUMO

The gastrointestinal tract is equipped with a highly specialized intrinsic immune system. However, the intestine is exposed to a high antigenic burden that requires a fast, nonspecific response -so-called innate immunity- to maintain homeostasis and protect the body from incoming pathogens. In the last decade multiple studies helped to unravel the particular developmental requirements and specific functions of the cells that play a role in innate immunity. In this review we shall focus on innate lymphoid cells, a newly discovered, heterogeneous set of cells that derive from an Id2-dependent lymphoid progenitor cell population. These cells have been categorized on the basis of the pattern of cytokines that they secrete, and the transcription factors that regulate their development and functions. Innate lymphoid cells play a role in the early response to pathogens, the anatomical contention of the commensal flora, and the maintenance of epithelial integrity.Amongst the various innate lymphoid cells we shall lay emphasis on a subpopulation with several peculiarities, namely that of natural killer T cells, a subset of T lymphocytes that express both T-cell and NK-cell receptors. The most numerous fraction of the NKT population are the so-called invariant NKT or iNKT cells. These iNKT cells have an invariant TCR and recognize the glycolipidic structures presented by the CD1d molecule, a homolog of class-I MHC molecules. Following activation they rapidly acquire cytotoxic activity and secrete both Th1 and Th2 cytokines, including IL-17. While their specific role is not yet established, iNKT cells take part in a great variety of intestinal immune responses ranging from oral tolerance to involvement in a number of gastrointestinal conditions.


Assuntos
Trato Gastrointestinal/imunologia , Imunidade Inata , Linfócitos/imunologia , Animais , Humanos , Linfócitos/classificação , Células T Matadoras Naturais/imunologia
11.
Rev. esp. enferm. dig ; 106(5): 334-345, mayo 2014. tab, ilus
Artigo em Inglês | IBECS | ID: ibc-128189

RESUMO

El tracto gastrointestinal está equipado con un sistema inmune intrínseco altamente especializado. Sin embargo, el intestino soporta una gran carga antigénica que requiere de una respuesta rápida e inespecífica, denominada inmunidad innata, para mantener la homeostasis y proteger al organismo de la entrada de patógenos. En la última década, numerosos estudios han contribuido a desentrañar los requisitos particulares de desarrollo y las funciones específicas de las células que intervienen en la inmunidad innata. En esta revisión, nos centraremos en las células linfoides innatas, un nuevo y heterogéneo grupo de células derivadas de una población linfoide progenitora Id2- dependiente. Estas células han sido categorizadas en base al patrón de citocinas que producen y los factores de transcripción que regulan su desarrollo y funciones. Las células linfoides innatas intervienen en la respuesta temprana contra agentes patógenos, la contención anatómica de la flora comensal, y el mantenimiento de la integridad epitelial. Dentro de las distintas células linfoides innatas haremos especial hincapié en una subpoblación con diversas particularidades, las células T natural killer, un subtipo de linfocitos T que expresan receptores de células T y NK. La fracción más numerosa de células NKT son las denominadas NKT invariantes o iNKT. Las células iNKT, poseen un TCR invariante y reconocen estructuras glicolípidicas presentadas por la molécula CD1d, homóloga de MHC de clase I. Tras su activación, adquieren rápidamente actividad citotóxica y producen citocinas tanto Th1 como Th2, e incluso IL-17. Aunque su papel concreto no está determinado, las células iNKT intervienen en una gran variedad de respuestas inmunes intestinales, desde la tolerancia oral hasta su implicación en diversas patologías del tracto gastrointestinal (AU)


The gastrointestinal tract is equipped with a highly specialized intrinsic immune system. However, the intestine is exposed to a high antigenic burden that requires a fast, nonspecific response –so-called innate immunity– to maintain homeostasis and protect the body from incoming pathogens. In the last decade multiple studies helped to unravel the particular developmental requirements and specific functions of the cells that play a role in innate immunity. In this review we shall focus on innate lymphoid cells, a newly discovered, heterogeneous set of cells that derive from an Id2-dependent lymphoid progenitor cell population. These cells have been categorized on the basis of the pattern of cytokines that they secrete, and the transcription factors that regulate their development and functions. Innate lymphoid cells play a role in the early response to pathogens, the anatomical contention of the commensal flora, and the maintenance of epithelial integrity. Amongst the various innate lymphoid cells we shall lay emphasis on a subpopulation with several peculiarities, namely that of natural killer T cells, a subset of T lymphocytes that express both T-cell and NK-cell receptors. The most numerous fraction of the NKT population are the so-called invariant NKT or iNKT cells. These iNKT cells have an invariant TCR and recognize the glycolipidic structures presented by the CD1d molecule, a homolog of class-I MHC molecules. Following activation they rapidly acquire cytotoxic activity and secrete both Th1 and Th2 cytokines, including IL-17. While their specific role is not yet established, iNKT cells take part in a great variety of intestinal immune responses ranging from oral tolerance to involvement in a number of gastrointestinal conditions (AU)


Assuntos
Humanos , Masculino , Feminino , Células Enteroendócrinas/imunologia , Trato Gastrointestinal/citologia , Trato Gastrointestinal/imunologia , Gastroenteropatias/diagnóstico , Gastroenteropatias/imunologia , Linfócitos/imunologia , Linfócitos/metabolismo , Linfócitos T/citologia , Linfócitos T/imunologia , Doenças Inflamatórias Intestinais/imunologia , Células Matadoras Naturais/imunologia , Células Matadoras Naturais/metabolismo , Doenças Inflamatórias Intestinais/diagnóstico , Doenças Inflamatórias Intestinais/fisiopatologia , Antígenos CD1d/uso terapêutico , Antígenos CD1d/imunologia
12.
PLoS One ; 7(2): e30791, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22319588

RESUMO

Interactions between environmental factors and predisposing genes could be involved in the development of coeliac disease (CD). This study has assessed whether milk-feeding type and HLA-genotype influence the intestinal microbiota composition of infants with a family history of CD. The study included 164 healthy newborns, with at least one first-degree relative with CD, classified according to their HLA-DQ genotype by PCR-SSP DQB1 and DQA1 typing. Faecal microbiota was analysed by quantitative PCR at 7 days, and at 1 and 4 months of age. Significant interactions between milk-feeding type and HLA-DQ genotype on bacterial numbers were not detected by applying a linear mixed-model analysis for repeated measures. In the whole population, breast-feeding promoted colonization of C. leptum group, B. longum and B. breve, while formula-feeding promoted that of Bacteroides fragilis group, C. coccoides-E. rectale group, E. coli and B. lactis. Moreover, increased numbers of B. fragilis group and Staphylococcus spp., and reduced numbers of Bifidobacterium spp. and B. longum were detected in infants with increased genetic risk of developing CD. Analyses within subgroups of either breast-fed or formula-fed infants indicated that in both cases increased risk of CD was associated with lower numbers of B. longum and/or Bifidobacterium spp. In addition, in breast-fed infants the increased genetic risk of developing CD was associated with increased C. leptum group numbers, while in formula-fed infants it was associated with increased Staphylococcus and B. fragilis group numbers. Overall, milk-feeding type in conjunction with HLA-DQ genotype play a role in establishing infants' gut microbiota; moreover, breast-feeding reduced the genotype-related differences in microbiota composition, which could partly explain the protective role attributed to breast milk in this disorder.


Assuntos
Doença Celíaca/etiologia , Comportamento Alimentar , Predisposição Genética para Doença , Intestinos/microbiologia , Metagenoma/genética , Aleitamento Materno , Doença Celíaca/genética , Doença Celíaca/microbiologia , Família , Genótipo , Antígenos HLA-DQ , Humanos , Lactente , Fórmulas Infantis , Recém-Nascido , Leite Humano
16.
Appl Environ Microbiol ; 77(15): 5316-23, 2011 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-21642397

RESUMO

Celiac disease (CD) is an immune-mediated enteropathy involving genetic and environmental factors whose interaction might influence disease risk. The aim of this study was to determine the effects of milk-feeding practices and the HLA-DQ genotype on intestinal colonization of Bacteroides species in infants at risk of CD development. This study included 75 full-term newborns with at least one first-degree relative suffering from CD. Infants were classified according to milk-feeding practice (breast-feeding or formula feeding) and HLA-DQ genotype (high or low genetic risk). Stools were analyzed at 7 days, 1 month, and 4 months by PCR and denaturing gradient gel electrophoresis (DGGE). The Bacteroides species diversity index was higher in formula-fed infants than in breast-fed infants. Breast-fed infants showed a higher prevalence of Bacteroides uniformis at 1 and 4 months of age, while formula-fed infants had a higher prevalence of B. intestinalis at all sampling times, of B. caccae at 7 days and 4 months, and of B. plebeius at 4 months. Infants with high genetic risk showed a higher prevalence of B. vulgatus, while those with low genetic risk showed a higher prevalence of B. ovatus, B. plebeius, and B. uniformis. Among breast-fed infants, the prevalence of B. uniformis was higher in those with low genetic risk than in those with high genetic risk. Among formula-fed infants, the prevalence of B. ovatus and B. plebeius was increased in those with low genetic risk, while the prevalence of B. vulgatus was higher in those with high genetic risk. The results indicate that both the type of milk feeding and the HLA-DQ genotype influence the colonization process of Bacteroides species, and possibly the disease risk.


Assuntos
Bacteroides , Aleitamento Materno , Doença Celíaca/genética , Doença Celíaca/microbiologia , Intestinos/microbiologia , Animais , Ingestão de Alimentos , Meio Ambiente , Fezes/microbiologia , Comportamento Alimentar , Antígenos HLA-DQ/genética , Humanos , Lactente , Alimentos Infantis , Fórmulas Infantis , Recém-Nascido , Leite , RNA Ribossômico 16S/análise , Fatores de Risco
17.
J Pediatr Gastroenterol Nutr ; 47 Suppl 1: S27-32, 2008 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-18667914

RESUMO

In susceptible individuals, the adaptive response, mediated by the activation of antigen-specific T lymphocytes, drives a proinflammatory response, which ends in an immune-mediated enteropathy characterized by villous atrophy, crypt hyperplasia, and recruitment of intraepithelial lymphocytes. In addition, some gluten peptides are able to induce an innate immune response in intestinal mucosa. The molecular mechanisms and the cells involved in the initial stages of the gluten-intestinal mucosa interaction are poorly understood to date. There is evidence of a direct toxic effect of gluten peptides in several biological models. However, the failure to control the inflammatory response may be one of the factors underlying gluten intolerance in these individuals. The cytokine network involved in celiac disease is characterized by abundant interferon-gamma in the intestinal mucosa. In addition, the production of interleukin (IL)-15, IL-18, and IL-21 is linked to gluten intake, which can drive the inflammatory response probably sustained by IL-18, IL-21, and perhaps IL-27 through STAT1 and STAT5 pathways, whereas neither IL-12 nor IL-23 plays a significant role in pathogenic mechanisms. Herein we describe the involvement of these activation pathways in the context of the pathogenesis of celiac disease.


Assuntos
Doença Celíaca , Citocinas/metabolismo , Imunidade Inata , Mediadores da Inflamação/metabolismo , Mucosa Intestinal/metabolismo , Linfócitos T/metabolismo , Doença Celíaca/imunologia , Doença Celíaca/metabolismo , Doença Celíaca/patologia , Criança , Pré-Escolar , Citocinas/imunologia , Feminino , Gliadina/imunologia , Glutens/imunologia , Humanos , Imunidade Celular , Imunidade nas Mucosas , Lactente , Mediadores da Inflamação/imunologia , Mucosa Intestinal/imunologia , Mucosa Intestinal/patologia , Masculino , Linfócitos T/imunologia
18.
Clin Immunol ; 126(2): 172-9, 2008 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-17974485

RESUMO

INTRODUCTION: A small proportion of coeliac disease (CD) patients become refractory (RCD) to a gluten-free diet (GFD) showing uncontrolled immune-mediated enteropathy. Some of these patients exhibit a high risk to develop enteropathy-associated T-cell lymphoma (EATL). AIM: The aim of the study was to find whether a lack of circulating homeostatic T cells, such as Treg, Tgammadelta(+) or iNKT cells would be associated with the development of RCD or EATL. PATIENTS AND METHODS: We investigated in a total of 137 CD patients [28 untreated, 80 responsive to GFD and 29 RCD (14 type I and 15 type II)] and 73 age-matched healthy volunteers the frequency of Treg, Tgammadelta(+) and iNKT lymphocytes by flow cytometric analysis of peripheral blood. RESULTS: Circulating Tgammadelta(+) cell and Treg frequencies in RCD were comparable to those in healthy controls. However, RCD patients had significantly reduced numbers of circulating iNKT cells, as compared to age-matched patients responding to a GFD. This reduction was similar in RCD patients with and without aberrant intraepithelial lymphocytes and in patients with EATL. Circulating iNKT cell numbers were not reduced in untreated coeliac patients. GFD treated patients had a significantly increased proportion of CD4(+) iNKT cells. CONCLUSION: Follow-up studies are necessary to determine whether CD4(+) iNKT cells control the immune response against gluten and their absence contributes to the progression to RCD and EATL.


Assuntos
Doença Celíaca/imunologia , Células Matadoras Naturais/imunologia , Linfoma de Células T/imunologia , Subpopulações de Linfócitos T/imunologia , Linfócitos T Reguladores/imunologia , Adolescente , Adulto , Idoso , Doença Celíaca/fisiopatologia , Criança , Pré-Escolar , Dieta , Feminino , Glutens/administração & dosagem , Glutens/efeitos adversos , Humanos , Lactente , Contagem de Linfócitos , Linfoma de Células T/metabolismo , Masculino , Pessoa de Meia-Idade
19.
Med. clín (Ed. impr.) ; 128(11): 401-406, mar. 2007. tab
Artigo em Espanhol | IBECS | ID: ibc-052908

RESUMO

Fundamento y objetivo: Es conocido el papel que desempeñan los mediadores inmunológicos proinflamatorios en la patogenia de algunas alteraciones de órganos distantes en la pancreatitis aguda (PA). El objetivo de este estudio ha sido evaluar la relación entre dichos mediadores y la afectación hepática, renal y pulmonar en pacientes con PA. Pacientes y método: En 34 pacientes con PA se valoraron el día del ingreso, parámetros bioquímicos de función hepática, creatinina y presión parcial de oxígeno (PO2) arterial, y se establecieron puntos de corte. Se determinaron el receptor soluble tipo I del factor de necrosis tumoral (sTNFRI), el receptor antagonista de la interleucina (IL) 1 (IL-1Ra), la IL-6, el receptor soluble de la IL-6 (sIL-6R), la IL-18 y la molécula de adherencia intercelular-1 (ICAM-1) los días 1, 2, 3 y 7, y se compararon entre los pacientes con los parámetros en el momento del ingreso (bioquímicos y PO2) superiores o inferiores a un punto de corte establecido. Resultados: Se encontraron valores significativamente más elevados y mantenidos de sTNFRI, IL-18 e ICAM-1, y de IL-6 sólo el primer día, en los pacientes con algún parámetro de función hepática superior al punto de corte. sTNFRI, IL-1Ra e ICAM-1 presentaban al inicio valores significativamente superiores en los pacientes en relación con la creatinina, y de éstos e IL-6 en los que presentaban PO2 inferior a 60 mmHg. Conclusiones: sTNFRI, IL-6, IL-18 e ICAM-1 se comportaron como marcadores tempranos de lesión hepática; sTNFRI, IL-1Ra e ICAM-1, de disfunción renal, y éstos e IL-6, de afectación pulmonar


Background and objective: There is a role of immunologic proinflammatory mediators in pathogenesis of distant organ disfunction in acute pancreatitis (AP). The aim is to evaluate the relationship between those mediators and liver, kidney and lung disfunction in patients with AP. Patients and method: On the day of admission in 34 patients with AP, biochemical parameters of liver function, cretinine and arterial partial pressure of oxygen (PO2) were determined, and cut points were established. Soluble tumor necrosis factor receptor I (sTNFRI), interleukin (IL) 1 receptor antagonist (IL-1Ra), IL-6, soluble IL-6 receptor (sIL-6R), IL-18, and intercellular adhesion molecule-1 (ICAM-1) were determined on days 1, 2, 3 and 7, and were compared between patients with biochemical parameters and PO2 on admission higher or lower than an established cut point. Results: Levels of sTNFRI, IL-18 and ICAM-1 were significantly higher and sustained, and IL-6 only the first day, in patients with parameters of liver function above the cut point. sTNFRI, IL-1Ra and ICAM-1 early showed significantly higher levels in relation with serum creatinine, and these and also IL-6 in those with PO2 below 60 mmHg. Conclusions: sTNFRI, IL-6, IL-18 and ICAM-1 behaved as early markers of hepatic alteration, sTNFRI, IL-1Ra and ICAM-1 of renal disfunction and these and IL-6 of lung injury


Assuntos
Humanos , Citocinas/análise , Pancreatite Necrosante Aguda/fisiopatologia , Mediadores da Inflamação/análise , Interleucina-6/análise , Interleucina-18/análise , Moléculas de Adesão Celular/análise , Testes de Função Hepática , Receptores do Fator de Necrose Tumoral/análise
20.
Med Clin (Barc) ; 127(4): 145-52, 2006 Jun 24.
Artigo em Espanhol | MEDLINE | ID: mdl-16831396

RESUMO

Inflammatory bowel disease (IBD) is produced by an exaggerated response to bacterial flora within the intestinal mucous, in which both environmental and genetic factors are involved. T lymphocytes are involved during the genesis and maintenance of IBD, and their cytokine profile in Crohn's disease (mostly Th1 cytokines) is different from that in ulcerative colitis (mainly Th2 cytokines). After the inflammatory response has been established, the balance between proinflammatory and regulatory cytokines determines the degree of mucosal damage and the form of presentation. A deeper knowledge of the immunological mechanisms involved in IBD has opened new research lines aimed to the development of new therapies such as the neutralization of proinflammatory cytokines with antibodies and the administration of antiinflammatory cytokines, which are currently at different stages of research.


Assuntos
Citocinas/fisiologia , Doenças Inflamatórias Intestinais/imunologia , Animais , Humanos , Imunidade Inata , Fatores Imunológicos/uso terapêutico , Doenças Inflamatórias Intestinais/tratamento farmacológico , Interleucina-2/fisiologia , Mucosa Intestinal/imunologia , Macrófagos , Linfócitos T/imunologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA