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The transition zone in Hirschsprung's bowel contains abnormal hybrid ganglia with characteristics of extrinsic nerves. | LitMetric

AI Article Synopsis

  • The study investigates short-segment Hirschsprung's disease, focusing on the aganglionic bowel region that lacks enteric ganglia yet has thickened nerve bundles (TNBs).
  • Researchers analyzed the cellular interactions between enteric ganglia and TNBs, finding abnormalities in the ganglia that are structurally influenced by TNBs in the transition zone between ganglionic and aganglionic gut segments.
  • The findings suggest that the unusual relationships between the enteric ganglia and TNBs may provide insights into the underlying mechanisms contributing to Hirschsprung’s disease.

Article Abstract

The aganglionic bowel in short-segment Hirschsprung's disease is characterized both by the absence of enteric ganglia and the presence of extrinsic thickened nerve bundles (TNBs). The relationship between the TNBs and the loss of enteric ganglia is unknown. Previous studies have described decreasing numbers of ganglia with increasing density of TNBs within the transition zone (TZ) between ganglionic and aganglionic gut, and there is some evidence of spatial contact between them in this region. To determine the cellular interactions involved, we have analysed the expression of perineurial markers of TNBs and enteric ganglionic markers for both neural cells and their ensheathing telocytes across four cranio-caudal segments consisting of most proximal ganglionic to most distal aganglionic from pull-through resected colon. We show that in the TZ, enteric ganglia are abnormal, being surrounded by perineurium cells characteristic of TNBs. Furthermore, short processes of ganglionic neurons extend caudally towards the aganglionic region, where telocytes in the TNB are located between the perineurium and nerve fibres into which they project telopodes. Thus, enteric ganglia within the TZ have abnormal structural characteristics, the cellular relationships of which are shared by the TNBs. These findings will help towards elucidation of the cellular mechanisms involved in the aetiology of Hirschsprung's disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9843525PMC
http://dx.doi.org/10.1111/jcmm.17659DOI Listing

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