Evidence for long-term sensitization of the bowel in patients with post-infectious-IBS.

Post-infectious irritable bowel syndrome (PI-IBS) is a common gastrointestinal disorder characterized by persistent abdominal pain despite recovery from acute gastroenteritis. The underlying mechanisms are unclear, although long-term changes in neuronal function, and low grade inflammation of the bowel have been hypothesized. We investigated the presence and mechanism of neuronal sensitization in a unique cohort of individuals who developed PI-IBS following exposure to contaminated drinking water 7 years ago. We provide direct evidence of ongoing sensitization of neuronal signaling in the bowel of patients with PI-IBS. These changes occur in the absence of any detectable tissue inflammation, and instead appear to be driven by pro-nociceptive changes in the gut micro-environment. This is evidenced by the activation of murine colonic afferents, and sensitization responses to capsaicin in dorsal root ganglia (DRGs) following application of supernatants generated from tissue biopsy of patients with PI-IBS. We demonstrate that neuronal signaling within the bowel of PI-IBS patients is sensitized 2 years after the initial infection has resolved. This sensitization appears to be mediated by a persistent pro-nociceptive change in the gut micro-environment, that has the capacity to stimulate visceral afferents and facilitate neuronal TRPV1 signaling

Efectos de los principales hongos cultivados en La Rioja en adipocitos humanos en cultivo

La obesidad es un grave problema de salud pública caracterizada por un aumento y mal funcionamiento del tejido adiposo. Por ello, el tejido adiposo constituye una diana interesante para establecer estrategias para prevenir o tratar la obesidad y sus co-morbilidades asociadas. En este sentido, uno de los grandes campos de investigación en la actualidad es el estudio de las propiedades de ciertos alimentos o nutrientes para combatir la obesidad y sus alteraciones metabólicas asociadas. Los hongos, y especialmente tres hongos cultivados en La Rioja (Agaricus bisporus, Pleurotus ostreatus, Lentinula edodes) parecen tener propiedades beneficiosas sobre la salud. No obstante, se desconocen sus efectos directos sobre el tejido adiposo. El objetivo de este trabajo fue analizar el efecto de estos hongos sobre el metabolismo glucídico y lipídico de adipocitos humanos en cultivo. También se analizaron sus efectos sobre la producción de dos adipoquinas producidas por los adipocitos con efectos sobre el control del peso corporal y la sensibilidad a la insulina. Nuestros resultados demuestran que los tres hongos presentan efectos directos y diferenciales entre sí sobre los adipocitos, siendo más potentes los efectos observados tras el tratamiento con P. ostreatus y L. edodes. También es importante resaltar que los resultados variaron dependiendo del origen de los adipocitos cultivados.Obesity is a serious public health problem characterized by an increased size of adipose tissue along with an important dysfunction of this fat depot. Thus, adipose tissue arises as an interesting target to prevent or treat obesity and its associated co-morbidities. There is growing interest in investigating the beneficial properties of certain foods or nutrients/ingredients to prevent and/or treat obesity and associated disorders. In this context, mushrooms and specially three mushrooms grown in La Rioja (Agaricus bisporus, Pleurotus ostreatus, Lentinula edodes) seem to exert beneficial actions in obesity and related disorders. However, the direct effects of these mushrooms on adipose tissue metabolism are still unknown. The aim of the present study was to analyze the direct effects of these mushrooms on glucose and lipid metabolism in human cultured adipocytes. Their actions on leptin and adiponectin, two adipokines with a key role in the control of body weight gain and insulin sensitivity, were also analyzed. Our results demonstrate that the three mushrooms have direct and differential effects on adipocytes, being the most powerful actions those observed after treatment with P. ostreatus and L. edodes. It is also worth mentioning that the results vary depending on the origin of the adipocytes

Local immune response to food antigens drives meal-induced abdominal pain

Up to 20% of people worldwide develop gastrointestinal symptoms following a meal1, leading to decreased quality of life, substantial morbidity and high medical costs. Although the interest of both the scientific and lay communities in this issue has increased markedly in recent years, with the worldwide introduction of gluten-free and other diets, the underlying mechanisms of food-induced abdominal complaints remain largely unknown. Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signalling resulted from histamine receptor H1-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation. Our results identify and characterize a peripheral mechanism that underlies food-induced abdominal pain, thereby creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders

Local immune response to food antigens drives meal-induced abdominal pain

Up to 20% of people worldwide develop gastrointestinal symptoms following a meal1, leading to decreased quality of life, substantial morbidity and high medical costs. Although the interest of both the scientific and lay communities in this issue has increased markedly in recent years, with the worldwide introduction of gluten-free and other diets, the underlying mechanisms of food-induced abdominal complaints remain largely unknown. Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signalling resulted from histamine receptor H1-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation. Our results identify and characterize a peripheral mechanism that underlies food-induced abdominal pain, thereby creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders

Local immune response to food antigens drives meal-induced abdominal pain

Up to 20% of people worldwide develop gastrointestinal symptoms following a meal(1), leading to decreased quality of life, substantial morbidity and high medical costs. Although the interest of both the scientific and lay communities in this issue has increased markedly in recent years, with the worldwide introduction of gluten-free and other diets, the underlying mechanisms of food-induced abdominal complaints remain largely unknown. Here we show that a bacterial infection and bacterial toxins can trigger an immune response that leads to the production of dietary-antigen-specific IgE antibodies in mice, which are limited to the intestine. Following subsequent oral ingestion of the respective dietary antigen, an IgE- and mast-cell-dependent mechanism induced increased visceral pain. This aberrant pain signalling resulted from histamine receptor H-1-mediated sensitization of visceral afferents. Moreover, injection of food antigens (gluten, wheat, soy and milk) into the rectosigmoid mucosa of patients with irritable bowel syndrome induced local oedema and mast cell activation. Our results identify and characterize a peripheral mechanism that underlies food-induced abdominal pain, thereby creating new possibilities for the treatment of irritable bowel syndrome and related abdominal pain disorders. In mice, oral tolerance to food antigens can break down after enteric infection, and this leads to food-induced pain resembling irritable bowel syndrome in humans