Would you like to see your presentation here, made available to a global audience of researchers?
Add your own presentation or have us affordably record your next conference.
Abstract Title Altered Mucin Expression Detected in the Pathogenesis of Necrotizing Enterocolitis Background Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease affecting premature infants, marked by severe intestinal inflammation, mucosal necrosis, and high mortality. The intestinal mucosal barrier, maintained in part by goblet cell–secreted mucins, plays a critical role in host defense and microbial containment. Disruption of this barrier has been implicated in NEC pathogenesis, yet the specific role of mucin subtype expression and goblet cell dynamics in human NEC tissue remains incompletely understood. We hypothesize that NEC is associated with both a quantitative reduction in goblet cells and qualitative alterations in mucin expression patterns. Method Human intestinal samples from confirmed NEC cases and matched controls were obtained from histological sections. Samples and regions with clear epithelium and intact mucosa were assessed. Goblet cell mucin composition was visualized using Alcian Blue/Periodic Acid-Schiff (AB/PAS) staining, which differentially stains acidic (cyan), neutral (magenta), and mixed (dark blue) mucins. Using ImageJ, high-resolution images were analyzed to quantify goblet cells per crypt and classify their mucin phenotype. Data were compiled in a quantitative spreadsheet and the total number of each goblet cell mucin type were compared to identify trends for future investigation. Results Quantitative analysis demonstrates a consistent downward trend in total goblet cell density in NEC samples compared to controls. Overall, there was a ~21.6% decrease in total goblet cell count. Notably, the most pronounced decline was in neutral mucin- producing goblet cells in NEC tissue, which exhibited ~81.8% decrease in NEC tissue. Mixed and acidic mucin-producing goblet cells showed smaller reductions of ~18.8% and ~13.5%, respectively, in NEC samples compared to controls. These findings suggest a selective alteration in mucin subtype expression. Mucin composition, particularly the dramatic loss of neutral mucins, may play a role in weakening the protective mucus layer, thus contributing to epithelial vulnerability and disease progression in NEC. Conclusion Our study provides evidence that NEC is associated with both quantitative and qualitative changes in goblet cell populations and mucin subtype expression. The selective depletion of neutral mucin-secreting goblet cells may compromise the integrity of the mucosal barrier, facilitating inflammation and microbial translocation. Ongoing analysis will incorporate additional samples and statistical modeling to confirm the significance of these trends. Future directions include expanding the sample size and assessing correlations with clinical outcomes. These findings emphasize the importance of mucin biology in NEC pathogenesis and may inform future therapeutic strategies aimed at restoring mucosal protection in at-risk infants.