Abstract
Very early onset inflammatory bowel disease (VEO-IBD) is characterized by multifactorial chronic recurrent intestinal inflammation. Compared with elderly patients, those with VEO-IBD have a more serious condition, not responsive to conventional treatments, with a poor prognosis. Recent studies found that genetic and immunologic abnormalities are closely related to VEO-IBD. Intestinal immune homeostasis monogenic defects (IIHMDs) are changed through various mechanisms. Recent studies have also revealed that abnormalities in genes and immune molecular mechanisms are closely related to VEO-IBD. IIHMDs change through various mechanisms. Epigenetic factors can mediate the interaction between the environment and genome, and genetic factors and immune molecules may be involved in the pathogenesis of the environment and gut microbiota. These discoveries will provide new directions and ideas for the treatment of VEO-IBD.
Highlights
Very early onset inflammatory bowel disease (VEO-IBD) refers to a subgroup of pediatric patients diagnosed with IBD before the age of 6 years [1]; it includes subclasses of infantIBD and neonatal IBD diagnosed before the age of 2 years and 28 days, respectively
In 2009, mutation of IL-10RA-IL-10RB was found in infants with IBD, providing a new comprehension of the pathogenesis of IBD [23], which is consistent with the conclusion of previous studies that the lack of an anti-inflammatory effect of IL-10 causes the activation of an explosive intestinal immune response
The most recent national case–control study from Sweden demonstrated a positive association between a Salmonella diagnosis and the likelihood of IBD, and this study found that Clostridium difficile was associated with higher rates of ulcerative colitis (UC) and Crohn’s disease (CD) [70]
Summary
Very early onset inflammatory bowel disease (VEO-IBD) refers to a subgroup of pediatric patients diagnosed with IBD before the age of 6 years [1]; it includes subclasses of infantIBD and neonatal IBD diagnosed before the age of 2 years and 28 days, respectively. In 2009, mutation of IL-10RA-IL-10RB was found in infants with IBD, providing a new comprehension of the pathogenesis of IBD [23], which is consistent with the conclusion of previous studies that the lack of an anti-inflammatory effect of IL-10 causes the activation of an explosive intestinal immune response. These mutations are associated with severe intestinal inflammation, especially in neonatal or infantile VEO-IBD with a phenotype of severe enterocolitis and perianal disease [24]. The use of antibiotics, in infancy, could lead to changes in the gut microbiota, suggesting they have a vital role in development of the immune system [77]
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