AI Article Synopsis

  • IBS (Irritable Bowel Syndrome) is a condition characterized by abdominal pain and varying bowel habits, particularly focusing on the diarrhea subtype (IBS-D), which shows changes in gut barrier and immune responses.
  • A study analyzed jejunal biopsies and stool samples from both IBS-D patients and healthy controls, measuring factors like plasma cell activation, nerve proximity, and glycocalyx thickness, finding notable differences in humoral immune pathways.
  • Results indicated that IBS-D patients had heightened plasma cell activity and lower glycocalyx thickness, linking these factors to gut dysfunction and clinical symptoms, suggesting the need for further research to clarify the mechanisms involved.

Article Abstract

Irritable bowel syndrome (IBS) is a disorder of brain-gut interaction characterised by abdominal pain and changes in bowel habits. In the diarrhoea subtype (IBS-D), altered epithelial barrier and mucosal immune activation are associated with clinical manifestations. We aimed to further evaluate plasma cells and epithelial integrity to gain understanding of IBS-D pathophysiology. One mucosal jejunal biopsy and one stool sample were obtained from healthy controls and IBS-D patients. Gastrointestinal symptoms, stress, and depression scores were recorded. In the jejunal mucosa, RNAseq and gene set enrichment analyses were performed. A morphometric analysis by electron microscopy quantified plasma cell activation and proximity to enteric nerves and glycocalyx thickness. Immunoglobulins concentration was assessed in the stool. IBS-D patients showed differential expression of humoral pathways compared to controls. Activation and proximity of plasma cells to nerves and IgG concentration were also higher in IBS-D. Glycocalyx thickness was lower in IBS-D compared to controls, and this reduction correlated with plasma cell activation, proximity to nerves, and clinical symptoms. These results support humoral activity and loss of epithelial integrity as important contributors to gut dysfunction and clinical manifestations in IBS-D. Additional studies are needed to identify the triggers of these alterations to better define IBS-D pathophysiology.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9265332PMC
http://dx.doi.org/10.3390/cells11132046DOI Listing

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