RESUMEN
BACKGROUND & AIMS: Non-celiac gluten sensitivity (NCGS) is characterized by intestinal and extra-intestinal symptoms triggered by ingestion of gluten. However, non-gluten triggers have recently been implicated, and a FODMAP (fermentable oligo-, di-, monosaccharides and polyols)-reduced diet can partially improve symptoms in NCGS. Our aim was to analyze the effect of a low FODMAP versus a gluten-free diet (GFD) on clinical symptoms, psychological well-being, intestinal inflammation and integrity, and stool microbiota. METHODS: Nineteen patients with NCGS and ten healthy controls consumed a gluten-containing standard diet before starting a two-week low FODMAP diet; after a five day transition period, participants ingested a GFD for another two weeks. The primary outcome measure was the improvement of clinical symptoms in NCGS patients under the different diets. Secondary outcomes were the determination of dietary effects on intestinal inflammation, psychological well-being, and differences in stool microbiota between NCGS patients and controls. RESULTS: The low FODMAP diet and especially the GFD led to a significant improvement of clinical and psychological symptoms in NCGS. A clear reduction in duodenal intraepithelial lymphocytes and mucin-producing Goblet cells was found after the GFD in these patients. Significant microbial differences between NCGS patients and controls were noticed in stool samples at every time point. Both diets caused microbial shifts in all participants, with a greater variability on genus level and metabolisms groups in NCGS patients. CONCLUSIONS: Our findings suggest a multifactorial etiology of NCGS, due to a functional effect caused by FODMAPs, combined with a mild gluten-triggered immune reaction, and a microbiota dysbalance. CLINICALTRIAL. GOV ID: NCT03268720.
Asunto(s)
Dieta Baja en Carbohidratos , Dieta Sin Gluten , Microbioma Gastrointestinal/fisiología , Síndromes de Malabsorción , Adulto , Estudios de Casos y Controles , Heces/microbiología , Femenino , Humanos , Síndromes de Malabsorción/dietoterapia , Síndromes de Malabsorción/fisiopatología , Masculino , Persona de Mediana Edad , Adulto JovenRESUMEN
Gut microbiota are permanent residents of humans with the highest concentrations being found in human colon. Humans get the first contact with bacteria at delivery, and microbiota are subject of permanent change during the life. The individual microbiota pattern is highly variable and varying environmental conditions, e.g., diets, antigen exposure, infections, or medication, as well as genetics, age, or hygiene factors, strongly influence the bacterial community. A fine interaction between the host and microbiota determines the outcome of health or disease. The gut immune system is constantly challenged to distinguish between commensal non-invasive bacteria and potential pathogens. Goblet cells produce mucins that prevent most gut bacteria from penetrating through intestinal epithelial barrier, and Paneth cells are the main supplier of anti-microbial defensins. Gut epithelial and immune cells recognize bacteria via surface markers and they initiate an adequate immune answer. A dysbiosis is noticed in several diseases, but the crucial role in pathogenesis has to be proven. Prebiotics or probiotics are discussed as valuable tools to preserve or restore a healthy gut community.
RESUMEN
BACKGROUND: Liver and intestine are in close contact with each other. The risk of damage to the liver increases, when the intestinal barrier is damaged ("leaky gut") . METHOD: The review article describes how intestinal bacteria influence the pathogenesis of chronic liver diseases and what treatment options are available. RESULTS AND CONCLUSIONS: Intestinal dysbiosis plays an important role in the development of chronic liver diseases such as alcoholic liver disease, nonalcoholic fatty liver disease, primary biliary cholangitis, primary sclerosing cholangitis, and cirrhosis. Intestinal microbial modulating therapy with probiotics, prebiotics or synbiotics shows positive effects. The more precise meaning of this therapeutic approach needs to be clarified in further studies.
Asunto(s)
Disbiosis , Microbioma Gastrointestinal , Intestinos , Hepatopatías , Hígado , Colangitis , Humanos , Intestinos/microbiología , Intestinos/fisiología , Intestinos/fisiopatología , Hígado/fisiología , Hígado/fisiopatología , Prebióticos , ProbióticosRESUMEN
Chronic liver diseases are a major cause of morbidity and mortality worldwide. Recently, gut dysbiosis was identified as an important factor in the pathogenesis of liver diseases. The relationship between gut microbiota and the liver is still not well understood; however, dysfunction of the gut mucosal barrier ("leaky gut") and increased bacterial translocation into the liver via the gutâ»liver axis probably play crucial roles in liver disease development and progression. The liver is an important immunological organ, and, after exposure to gut-derived bacteria via portal circulation, it responds with activation of the innate and adaptive immune system, leading to hepatic injury. A better understanding of the pathophysiological links among gut dysbiosis, the integrity of the gut barrier, and the hepatic immune response to gut-derived factors is essential for the development of new therapies to treat chronic liver diseases.