ArticleJournal of pediatric surgery2010
Murine model of Hirschsprung-associated enterocolitis II: Surgical correction of aganglionosis does not eliminate enterocolitis.
Article in Journal of pediatric surgery, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Early intervention in Hirschsprung's disease: effects on enterocolitis and surgical outcomes.BMC pediatrics · 2024Article
- Neonatal development of intestinal neuroimmune interactions.Trends in neurosciences · 2022Review
- Current understanding of Hirschsprung-associated enterocolitis: Pathogenesis, diagnosis and treatment.Seminars in pediatric surgery · 2022Review
- Surgical method to prevent early death of neonatal rat pups with Hirschsprung disease, thus permitting development of long-term therapeutic approaches.Biology methods & protocols · 2022Article
- Intestinal proinflammatory macrophages induce a phenotypic switch in interstitial cells of Cajal.The Journal of clinical investigation · 2020Article
- Bacterial Microbiome Dynamics in Post Pull-Through Hirschsprung-Associated Enterocolitis (HAEC): An Experimental Study Employing the Endothelin Receptor B-Null Mouse Model.Frontiers in surgery · 2018Article
- Established and emerging concepts in Hirschsprung's-associated enterocolitis.Pediatric surgery international · 2016Review
- Isogenic enteric neural progenitor cells can replace missing neurons and glia in mice with Hirschsprung disease.Neurogastroenterology and motility · 2016Article
- Surgical Intervention to Rescue Hirschsprung Disease in a Rat Model.Journal of neurogastroenterology and motility · 2015Article
- Hirschsprung's associated enterocolitis.Current opinion in pediatrics · 2015Review
- Enterocolitis causes profound lymphoid depletion in endothelin receptor B- and endothelin 3-null mouse models of Hirschsprung-associated enterocolitis.European journal of immunology · 2015Article
- Impaired Cellular Immunity in the Murine Neural Crest Conditional Deletion of Endothelin Receptor-B Model of Hirschsprung's Disease.PloS one · 2015Article
- Enteric neuron imbalance and proximal dysmotility in ganglionated intestine of theCellular and molecular gastroenterology and hepatology · 2015Article
- Balancing on the crest - Evidence for disruption of the enteric ganglia via inappropriate lineage segregation and consequences for gastrointestinal function.Developmental biology · 2013Review
- Recent developments in Hirschsprung's-associated enterocolitis.Current gastroenterology reports · 2013Review
- Multiphoton microscopy to identify and characterize the transition zone in a mouse model of Hirschsprung disease.Journal of pediatric surgery · 2013Article
- Splenic lymphopenia in the endothelin receptor B-null mouse: implications for Hirschsprung associated enterocolitis.Pediatric surgery international · 2011Article
- Imaging the Gastrointestinal Tract of Small Animals.Journal of neuroparasitology · 2010Article
- Mortality Prediction Score for Hirschsprung's Disease-Associated Enterocolitis: A Novel Mortality Prediction Model.Journal of Indian Association of Pediatric SurgeonsArticle
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundHirschsprung disease (HD) results from aganglionosis of the colon, is linked to acute and chronic enterocolitis (known as Hirschsprung-associated enterocolitis) despite successful corrective surgery, and can lead to bacteremia and even death. The genetic and molecular mechanisms underlying these disorders are largely unknown.
methodsWe developed a microsurgical corrective pull-through procedure in mice, and applied that to Ednrb(-/-) mice, which manifest aganglionic megacolon that is very similar to HD. Wild-type littermates (Ednrb(+/+)) also underwent identical surgery. At prespecified time points postoperatively, mice were sacrificed, and histopathologic analyses of intestinal inflammation were performed. Mice of both genotypes were sacrificed after the postoperative recovery period to determine if corrective surgery itself caused inflammation. Stooling patterns were assessed as well to determine if intestinal function normalized after surgery.
resultsThere was no difference in histopathological enterocolitis scores after recovery from surgery. Stooling patterns in Ednrb(-/-) and Ednrb(+/+) mice were similar postoperatively, suggesting normalization of intestinal function. However, with time, approximately 40% of Ednrb(-/-) mice developed clinical illness consistent with enterocolitis. No control (Ednrb(+/+)) mice developed clinical enterocolitis. Histopathological enterocolitis scores in the 40% of Ednrb(-/-) mice that developed clinical enterocolitis postoperatively were significantly worse than those of healthy postoperative Ednrb(-/-) mice. In contrast, none of the Ednrb(+/+) control mice exhibited postoperative long-term inflammation.
conclusionsMicrosurgical pull-through operation in Ednrb(-/-) mice produces a mouse model that closely resembles key features of Hirschsprung-associated enterocolitis, enabling controlled study of genetic and molecular mechanisms in Ednrb(-/-) mice and other genotypes that produce similar phenotypes.
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