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Cross-talk between intestinal epithelial cells and immune cells in inflammatory bowel disease
Sara Al-Ghadban1, Samira Kaissi1, Fadia R Homaidan2
1Department of Anatomy, Cell Biology, and Physiological Sciences, Faculty of Medicine, American university of Beirut, Beirut, Lebanon.
Insights
Inflammatory bowel disease (IBD) disrupts the intestinal barrier by altering communication between intestinal epithelial cells (IECs) and macrophages (MΦ). This interaction affects key junctional proteins, contributing to barrier dysfunction.
Area of Science:
- Gastroenterology
- Cell Biology
- Immunology
Background:
- Inflammatory bowel disease (IBD) is characterized by intestinal epithelial cell (IEC) dysfunction and inflammatory cell infiltration.
- The interplay between IECs and macrophages (MΦ) in IBD pathogenesis is not fully understood.
- Intercellular communication mechanisms, including gap junctions, may play a role in IBD.
Purpose of the Study:
- To investigate the reciprocal interactions between human IECs and MΦ in a co-culture system relevant to IBD.
- To examine the expression and localization of intercellular junctional proteins in IECs under inflammatory conditions and in IBD patient tissues.
- To elucidate the role of cell-cell communication in regulating the intestinal epithelial barrier during inflammation.
Main Methods:
- Co-culture system of human IECs and MΦ to mimic IBD conditions.
- Investigation of intercellular junctional protein expression (Connexins, E-cadherin, ZO-1, β-catenin) via cell culture and patient tissue analysis.
- Assessment of protein localization and association with basement membrane components like collagen type IV.
Main Results:
- IECs form functional gap junctions with both IECs and MΦ.
- Inflammatory conditions increase Connexin (Cx26, Cx43) expression in cultured IECs.
- IBD tissues show altered Cx26 and Cx43 localization to the basal membrane, correlating with decreased E-cadherin, ZO-1, β-catenin, and collagen type IV, alongside MΦ infiltration.
Conclusions:
- Paracrine and direct cell-cell communication between IECs and MΦ significantly impacts IEC function.
- Altered junctional complexes and protein redistribution contribute to the dysregulation of the intestinal epithelial barrier in IBD.
- Hetero-cellular communication via junctional complexes is a key factor in IBD-associated barrier defects.
Abstract:
Inflammatory bowel disease (IBD) involves functional impairment of intestinal epithelial cells (IECs), concomitant with the infiltration of the lamina propria by inflammatory cells. We explored the reciprocal paracrine and direct interaction between human IECs and macrophages (MΦ) in a co-culture system that mimics some aspects of IBD. We investigated the expression of intercellular junctional proteins in cultured IECs under inflammatory conditions and in tissues from IBD patients. IECs establish functional gap junctions with IECs and MΦ, respectively. Connexin (Cx26) and Cx43 expression in cultured IECs is augmented under inflammatory conditions; while, Cx43-associated junctional complexes partners, E-cadherin, ZO-1, and β-catenin expression is decreased. The expression of Cx26 and Cx43 in IBD tissues is redistributed to the basal membrane of IEC, which is associated with decrease in junctional complex proteins' expression, collagen type IV expression and infiltration of MΦ. These data support the notion that the combination of paracrine and hetero-cellular communication between IECs and MΦs may regulate epithelial cell function through the establishment of junctional complexes between inflammatory cells and IECs, which ultimately contribute to the dys-regulation of intestinal epithelial barrier.
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