Role of brain-gut axis in mechanism of gastrointestinal defense.

The digestive system, comprising gastrointestinal (GI)-tract and connecting organs, such as liver or pancreas, has a wide autonomy in the human body due to the presence of specific nervous and endocrine systems of its own and can act voluntarily without stimulation from the rest of the body. This wide physiological autonomy of a digestive tract does not exclude connection with other organs and central as well as peripheral mechanisms controlling nervous and hormonal systems. The vagal nerve is a structure connecting GI-tract with brain centers. Both, the afferent and efferent components of the vagal nerve innervate the GI-tract and modify its functions. An example of stimulants affecting afferent fibers of vagal nerve are digestive hormones, such as cholecystokinin (CCK), because CCK is commonly recognized as the gut hormone that stimulates specific receptors located at the endings of vagal afferent fibers and promotes the vago-vagal reflex. Recent studies have documented that GI-tract is a source of abundant hormones regulating the hunger - satiety centers in the hypothalamus via afferent fibers of the vagal nerve, forming the brain-gut axis. In addition, local endocrine cells in the GI-tract can produce biogenic amines, such as serotonin or histamine which also can stimulate afferent component of this axis. The complexity of brain - gut axis is augmented by the participation of other factors, that can influence it, such as metabolites of gut microbiota, changes in the intestinal permeability, the proinflammatory cytokines and other immune responses, activity of the stress hormones, such as adrenaline, cortisol and aldosterone. In addition, the presence of the short chain fatty acids (SCFA) can modify the bidirectional brain-gut and gut-brain axes activity, indirectly, as nutrients for specific bacterial species, or directly, by stimulation of the specific receptors located within the GI wall. In this review, we focused on the brain-gut axis is involved in the strenghtening of the mucosal barrier via maintaining of oxidative balance. The main process reaction causing cellular destruction is lipid peroxidation. Lipid peroxides disrupt the structure of cellular lipids, making this barrier more permeable. Increased cellular permeability of GI-tract barrier contributes to the stimulation of the brain-gut axis. Pharmacological agents, affecting mucosal blood flow, such as cyclooxygenase (COX) products, COX inhibitors and pentoxifylline, are also able to modify functions of the brain-gut axis. We conclude that brain-gut axis plays a particularly important role in maintaining of mucosal barrier in GI-tract and alteration in its functions is implicated in pathogenesis of various diseases of the gut.