ArticleLaboratory investigation; a journal of technical methods and pathology2026
Tight Junction Defects in Aganglionic and Ganglionic Colon in Children With Hirschsprung Disease.
Article in Laboratory investigation; a journal of technical methods and pathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Intestinal epithelial barrier loss has been suggested as a pathogenic factor in Hirschsprung-associated enterocolitis and intestinal dysfunction in children with Hirschsprung disease (HD), but there is a paucity of comprehensive studies on the tight junction proteins that regulate paracellular permeability in this population. This case-control study aimed to determine if colonic epithelial tight junction protein expression is altered in children with HD. We use quantitative immunofluorescence microscopy to assess the expression of tight junction proteins (claudin-1, claudin-2, claudin-3, claudin-4, claudin-7, claudin-15, ZO-1, ZO-2, and occludin) in 29 children with HD who underwent surgical reconstruction and 16 controls who underwent transmural colorectal surgical resection for other etiologies between January 2015 and December 2021. We found that the expression of claudin-2, claudin-15, and occludin was reduced in both ganglionic and aganglionic colon specimens from children with HD compared with controls. Expression of other tight junction proteins did not differ between the groups. Together with previous studies, these data suggest that decreased expression of paracellular Na
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