Epithelial cells in the intestine constitute a single cell layer that serves as a critical barrier against pathogen invasion into the host and also serves the critical functions of absorption of nutrients and/or secretion of biological compounds and water. This tissue is extremely complex, but many reviews explain the architecture.
During inflammatory bowel disease (IBD), there is increased inflammatory cytokines present in the tissue. This inflammation is correlated with increased permeability of the intestinal epithelium. The increased permeability is a dysfunctional barrier and thus increased antigen can pass into the host tissue and elicit chronic inflammation. To study the molecular mechanisms of this increased permeability, Wang et al use a cell culture model system to break down the signaling pathway leading to regulation of the barrier function, or epithelium permeability. The results show that the process essentially bottlenecks at the regulation of Myosin Light Chain Kinase (MLCK), a kinase shown to be responsible for actomyosin ring contraction which regulates permeability.
The results of Wang et al show that the regulation of MLCK is NFkB independent. Other studies show that NFkB could be involved but Wang et al present compelling and thorough evidence and back up their data with other evidences from the work of different labs. Overall I thought this was an excellent paper, progressing clearly though the experiments and clearly explaining the current models.
image from the BBC
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