About this Research Topic
Tight junctions regulate the permeability of ions, nutrients, and water through epithelial cell layers. The tight junctions are maintained by a complex network of protein interactions to establish a selectively permeable barrier to support absorption of nutrients and secretion of waste while preventing intrusion by luminal content. The integrity of tight junctions is regulated by the interaction between peripheral membrane adaptor proteins zonula occludens-1 (ZO-1), ZO-2, and ZO-3 that connect four integral transmembrane proteins, occludin, claudins, junctional adhesion molecule (JAM), and tricellulin to the actin cytoskeleton and to other signalling proteins. The distribution, expression levels and modification of tight junction proteins regulate the tight junction barrier. In addition, tight junctions are also regulated by intracellular signal transduction pathways. Dysfunction of tight junctions is associated with metabolic and inflammatory diseases. Nutritional factors on the other hand have been shown to improve the integrity of tight junctions.
While many proteins that form the paracellular pores have been reported, the influence of gene expression network, non-coding RNA, dietary components, and small molecules on the regulation of the permeability of the tight junctions and on the expression and distribution of those proteins and regulating the epithelial permeability is not well understood. In addition, there are limited studies on the influence of dietary input on the organ-specific features of tight junction-dependent barrier function. Food and nutritional supplements also contain components that induce inflammatory responses. Inflammatory cytokines such as tumor necrosis factor and interleukins has been shown to influence the expression of tight junction proteins. However, limited progress has been made to understand the influence of inflammatory responses to different components of food on the regulation of tight junction permeability. Therefore, this research topic aims to explore the influence of dietary nutrients and oral nutritional supplements such as phytochemicals on the regulation of tight junction permeability. Further understanding of the influence of dietary intake on the regulation of tight junctions can shed light on enhancing tight junction permeability to small polar compounds such as phenolic antioxidants and small molecule drugs and modulate inflammatory responses and related diseases.
We invite submission of manuscripts on original research, brief research reports, and review articles, that address regulation of tight junction permeability including regulation by dietary nutrients in different epithelial cell layers. Following are a short list of suggested themes. However, the scope of the research topic is not limited to the list of themes given below:
• regulation of passive paracellular permeation
• Influence of dietary nutrients such as fatty acids on passive paracellular permeation.
• Influence of components of food on the distribution, expression, and modifications of tight junction proteins, regulatory proteins, and regulatory RNA.
• Influence of components of food on signalling and inflammatory responses to and from tight junctions, adherens junctions, desmosomes, and gap junctions
• Dietary influence on dysregulation of tight junction barrier functions.
While many proteins that form the paracellular pores have been reported, the influence of gene expression network, non-coding RNA, dietary components, and small molecules on the regulation of the permeability of the tight junctions and on the expression and distribution of those proteins and regulating the epithelial permeability is not well understood. In addition, there are limited studies on the influence of dietary input on the organ-specific features of tight junction-dependent barrier function. Food and nutritional supplements also contain components that induce inflammatory responses. Inflammatory cytokines such as tumor necrosis factor and interleukins has been shown to influence the expression of tight junction proteins. However, limited progress has been made to understand the influence of inflammatory responses to different components of food on the regulation of tight junction permeability. Therefore, this research topic aims to explore the influence of dietary nutrients and oral nutritional supplements such as phytochemicals on the regulation of tight junction permeability. Further understanding of the influence of dietary intake on the regulation of tight junctions can shed light on enhancing tight junction permeability to small polar compounds such as phenolic antioxidants and small molecule drugs and modulate inflammatory responses and related diseases.
We invite submission of manuscripts on original research, brief research reports, and review articles, that address regulation of tight junction permeability including regulation by dietary nutrients in different epithelial cell layers. Following are a short list of suggested themes. However, the scope of the research topic is not limited to the list of themes given below:
• regulation of passive paracellular permeation
• Influence of dietary nutrients such as fatty acids on passive paracellular permeation.
• Influence of components of food on the distribution, expression, and modifications of tight junction proteins, regulatory proteins, and regulatory RNA.
• Influence of components of food on signalling and inflammatory responses to and from tight junctions, adherens junctions, desmosomes, and gap junctions
• Dietary influence on dysregulation of tight junction barrier functions.
Keywords: tight junctions, occluding junctions, zonulae occludentes, tight junction permeability, passive paracellular permeation, intestinal absorption, permeability of polar molecules
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
