1,721,076 research outputs found
Patent number WO 2012/017466 A1: USE OF HMGB1 AS A BIOLOGICAL MARKER OF BOWEL INFLAMMATORY CONDITIONS, NON-INVASIVE METHOD FOR ITS DETECTION IN FECAL SAMPLES AND KIT THEREOF
No full textInteractions Between Intestinal Microbiota and Innate Immune System in Pediatric Inflammatory Bowel Disease
No full textInflammatory bowel disease (IBD) is the result of an altered immune homeostasis within the intestinal mucosa against the gut microbiota, leading to chronic inflammation in genetically predisposed individuals. Under normal conditions, the immune system defends against pathogens and prevents the passage of excessive intestinal bacteria; regulatory pathways must maintain a low-grade, controlled inflammation in a healthy gut, but also induce a protective response against pathogens. The innate immune system is the first-line defense from microbes; dendritic cells, macrophages, and epithelial cells produce an initial, immediate response. The immune system constantly controls commensal bacteria and utilizes constitutive antimicrobial mechanisms to sustain immune homeostasis. The discovery that several genes linked to IBD modulate microbial recognition and innate immune pathways, such as nucleotide oligomerization domain 2 (Nod2), and genes that mediate autophagy (ie, ATG16L1, IRGM), has highlighted the critical role of host-microbe interactions in controlling intestinal immune homeostasis. Commensal microorganisms actively interact with the intestinal mucosa and influence the activity of the immune system as well as the amplitude of the immune response. In contrast, host factors can influence microbes, which in turn modulate disease susceptibility. In this paper, we focus on the mechanisms that mediate host-microbe interactions and how the disruption of this balance leads to chronic intestinal inflammation in IBD.Inflammatory bowel disease (IBD) is the result of an altered immune homeostasis within the intestinal mucosa against the gut microbiota, leading to chronic inflammation in genetically predisposed individuals. Under normal conditions, the immune system defends against pathogens and prevents the passage of excessive intestinal bacteria; regulatory pathways must maintain a low-grade, controlled inflammation in a healthy gut, but also induce a protective response against pathogens. The innate immune system is the first-line defense from microbes; dendritic cells, macrophages, and epithelial cells produce an initial, immediate response. The immune system constantly controls commensal bacteria and utilizes constitutive antimicrobial mechanisms to sustain immune homeostasis. The discovery that several genes linked to IBD modulate microbial recognition and innate immune pathways, such as nucleotide oligomerization domain 2 (Nod2), and genes that mediate autophagy (ie, ATG16L1, IRGM), has highlighted the critical role of host-microbe interactions in controlling intestinal immune homeostasis. Commensal microorganisms actively interact with the intestinal mucosa and influence the activity of the immune system as well as the amplitude of the immune response. In contrast, host factors can influence microbes, which in turn modulate disease susceptibility. In this paper, we focus on the mechanisms that mediate host-microbe interactions and how the disruption of this balance leads to chronic intestinal inflammation in IBD
Evaluation of chromosome painting to assess the induction and persistence of chromosome aberrations in mouse bone marrow cells by chemical agents
No full textFluorescence in situ hybridization with chromosome-specific painting probes (FISH painting) has been successfully applied to detect radiation-induced stable aberrations in humans and mice, whereas a few mouse studies with chemicals mostly failed to show any increase in chromosome-painting-detectable changes, especially in bone marrow cells. To further explore the feasibility of the painting approach to detect chemically induced stable aberrations, we treated mice with a single high dose of benzene, a potent bone-marrow-targeting clastogenic chemical and sacrificed them 24, 36h or 15 days later to collect bone marrow cells and analyze chromatid- and chromosome-type aberrations by FISH painting. In addition, we treated another group of mice with 18 daily low doses to show the potential for aberration induction and accumulation under chronic exposure. Chromatid-type aberrations were significantly increased 24 and 36h after acute treatment while chromosome-type ones were elevated above control values 36h and 15 days after exposure, showing that at least part of benzene-induced chromatid exchanges were converted into potentially stable chromosome aberrations. The most common aberration was an extra copy of one painted chromosome in a metaphase with the euploid number of centromeres which was interpreted as the consequence of a symmetric recombination between pericentromeric regions of one painted and one unpainted chromatid. Under chronic exposure, neither chromosome- nor chromatid-type aberrations were significantly elevated over control values, suggesting that the probability of enough primary lesions and secondary DNA double strand breaks occurring close enough together in time to allow chromosome exchanges to form is a critical limiting factor especially in a cycling cell population
Ulcerative colitis: Paediatric ulcerative colitis--can we predict proctocolectomy?
No full textGiven the early onset of ulcerative colitis in children, it is desirable to identify young patients with this disease who are at risk of adverse outcomes. Identification of these patients would enable the introduction of disease-modifying therapies early in the disease course and thus prevent the need for surgical therapy.Given the early onset of ulcerative colitis in children, it is desirable to identify young patients with this disease who are at risk of adverse outcomes. Identification of these patients would enable the introduction of disease-modifying therapies early in the disease course and thus prevent the need for surgical therapy
Incidence in pediatric IBD is rising: Help from health administrative data
No full text[No abstract available
USE OF THE RHO GDP DISSOCIATION INHIBITOR 2 PROTEIN AS A DIAGNOSTIC AND PROGNOSTIC MARKER OF INTESTINAL INFLAMMATORY DISEASES
No full textLa presente invenzione è diretta all’utilizzo diagnostico, prognostico e di risposta alla terapia della proteina inibitore 2 della dissociazione del Rho GDP per individuare condizioni di infiammazione intestinale cronica (con particolare riferimento alle Malattie Infiammatorie Croniche Intestinali (MICI), note internazionalmente come Inflammatory Bowel Disease (IBD)), nell’uomo. In particolare si descrive un metodo non invasivo per misurare uno stato infiammatorio intestinale nell’uomo attraverso la determinazione della presenza e della concentrazione della proteina inibitore 2 della dissociazione del Rho GDP in estratti fecali
Mucosal healing in Crohn's disease: new insights
No full textIntroduction: Traditional management of patients with Crohn's disease includes symptoms and quality of life improvement. With the advent of biological agents, mucosal healing has become an achievable goal, documented through endoscopy. However, due to the transmural nature of inflammation, the prevention of bowel damage should be included in the aims of a targeted therapeutic strategy.Areas covered: Updated literature has been searched in PubMed from 2008 to 2020. This review focuses on the state of the art in the innovative therapeutic goals in Crohn's disease, also considering still controversial aspects and future research topics in the management of Crohn's disease.Expert opinion: Although a widely agreed view supports the notion that mucosal healing and bowel damage control may promote beneficial outcomes (i.e. reduction in hospitalization and surgical rates, avoidance of steroids), long-term robust data are still missing. On the other hand, the development of -omics techniques has expanded our knowledge of the pathogenetic mechanism underlying inflammatory bowel disease and opened up new horizons in precision or personalized medicine
Apoptosis, necrosis, and necroptosis in the gut and intestinal homeostasis
Full text linkIntestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu
and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota.Moreover, IECs are strongly
involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death
in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The
emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This
review is focused on previous reports on different forms of cell death in intestinal epitheliumIntestinal epithelial cells (IECs) form a physiochemical barrier that separates the intestinal lumen from the host’s internal milieu
and is critical for electrolyte passage, nutrient absorption, and interaction with commensal microbiota.Moreover, IECs are strongly
involved in the intestinal mucosal inflammatory response as well as in mucosal innate and adaptive immune responses. Cell death
in the intestinal barrier is finely controlled, since alterations may lead to severe disorders, including inflammatory diseases. The
emerging picture indicates that intestinal epithelial cell death is strictly related to the maintenance of tissue homeostasis. This
review is focused on previous reports on different forms of cell death in intestinal epitheliu
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