[Significance of nervous system in inflammatory disease of the gut].

The review is dedicated to the role of sensory nerve endings of the gut, vegetal and central nervous system (CNS) in the diseases of gastrointestinal tract. Molecular-cellular inter-relations of nerve endings of the gut and neurons of the CNS are a key axis that among with neuroendocrine and immune responses, define the clinical manifestation and rehabilitation potential of the patient in the development of infectious process in the gut. Infectious-inflammation processes in the gut of various etiologies promote the increase of permeability of the intestine barrier with consequent trans-intestinal translocation of toxins and molecular mediators of inflammation to the system bloodstream. Bacterial toxins including LPS and cytokine imbalance induce microglia damage that defines destabilization of the barrier and vulnerability of neurons. The consequence is the inadequate reaction from autonomous nervous system with the development of uncontrolled abdominal spasms and increasing muscular atrophy. Toxemia at the same time promotes the increase of hematoencephalic barrier permeability, intake of inflammatory cytokines into the brain that induce inflammation in the brain periventricular areas with the development of intestinal encephalopathy. The assumed pathogenetic mechanism dictates a new therapy strategy that is mainly directed at brain protection: administration of etiotropic and anti-inflammatory drags, myotropic spasmolytics and various neuroprotectors.