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Marcello Chieppa, Alex Huang, Maria Rescigno, Ronald N. Germain, Intravital 2-Photon Microscopy of Dendritic Cell Extension Sampling Pathogen Bacteria Into the Small Bowel Lumen, Inflammatory Bowel Diseases, Volume 12, Issue suppl_2, 1 April 2006, Page S20, https://doi.org/10.1097/0054725-200604002-00042
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Background
Increasing evidence suggests that the pathogenesis of inflammatory bowel disease (IBD) can be determined by genetic factors together with mucosal immune deregulation. Bacteria that reside in the intestinal tract and contribute, under normal conditions, to the viability of the host can become, in patients with IBD, a source of continuous inflammation. An important immune cell type that could participate in the onset and development of IBD is represented by dendritic cells (DCs), the most important antigen-presenting cells. Under physiological conditions, DCs that reside in close contact with the intestinal epithelium are "educated" to be anti-inflammatory DCs that preserve the ability to capture and present antigens but lose the ability to drive a TH1 inflammatory response even after bacterial encounter. Understanding how DCs handle bacteria at mucosal surfaces is therefore crucial to determine whether deregulation of this pathway is involved in IBD pathology.
A previous in vitro study using a model epithelial cell line first revealed the capacity of DCs on the basolateral (ablumenal) side of the epithelium to extend processes across the tight junctions between these cells and capture bacteria from the apical (lumenal) side. This extension occurred without compromising the integrity of the epithelial barrier as a result of the creation of a tight junction-like structure between the dendrites and the contiguous epithelial cells. Later investigation also identified fractalkine (CX3CL1) made by the epithelial cells as playing a key role in promoting subepithelial DC localization and showed that DC acquired bacteria from the gut lumen when fractalkine signaling was present. Here we extend these prior studies on the capacity of lamina propria DCs to extend processes across the epithelium without breaching the tight junction barrier.
