Abstract
Important functions of intestinal epithelial cells (IECs) include enabling nutrient absorption to occur passively and acting as a defense barrier against potential xenobiotic components and pathogens. A compromise to IEC function can result in the translocation of bacteria, toxins, and allergens that lead to the onset of disease. Thus, the maintenance and optimal function of IECs are critically important to ensure health. Endogenous biosynthesis of nitric oxide (NO) regulates IEC functionality both directly, through free radical activity, and indirectly through cell signaling mechanisms that impact tight junction protein expression. In this paper, we review the current knowledge on factors that regulate inducible nitric oxide synthase (iNOS) and the subsequent roles that NO has on maintaining IECs’ intestinal epithelial barrier structure, functions, and associated mechanisms of action. We also summarize important findings on the effects of bioactive dietary food components that interact with NO production and affect downstream intestinal epithelium integrity.
Highlights
Intestinal epithelial cells (IECs) exist as a continuous layer of cells that line the surface of the intestinal epithelium and display important roles in the digestion of food and the absorption of nutrients
nitric oxide (NO) modulates the intestinal epithelial cell tight junction by altering the glutathione (GSH)/GSSG balance that results in the inactivation of phosphatases and protein tyrosine phosphorylation
A moderate amount of NO is continuously produced by NOS1 and NOS3, both of which are constitutively expressed in intestinal epithelial cells [8]
Summary
Intestinal epithelial cells (IECs) exist as a continuous layer of cells that line the surface of the intestinal epithelium and display important roles in the digestion of food and the absorption of nutrients. NO has a protective role against intestinal barrier dysfunction, brought on by oxidative stress that includes hydrogen peroxide-induced changes in the protein tyrosine phosphorylation of IECs [5]. NO modulates the intestinal epithelial cell tight junction by altering the glutathione (GSH)/GSSG balance that results in the inactivation of phosphatases and protein tyrosine phosphorylation. Intracellular pathways of cell signaling are sensitive to redox changes via the modification of enzymes altered by NO. Some examples of this include the oxidation of glutathione, the inactivation of protein phosphatases directly reacting with protein and lipid radicals, and sequestering metal cofactors which deactivate enzymes. A balanced redox status is paramount for the maintenance of protein structure, such as those that comprise tight junctions that enable intestinal cell functionality
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