Perspectives for pathogenetic therapy under impared gut-brain axis
Immunoinflammatory and neurohumoral mechanisms of diseases associated with the pathology of enteric brain axis are considered - from the acute local to the systemic chronic. Inflammation of the gastrointestinal tract (IBD) is the first sign of autonomic nervous system failure, because one of its basic reasons is considered to be the stress with hypothalamic-pituitary-adrenal pathway disturbance, increased cortisol synthesis and amplification of the inflammatory response with impaired permeability barrier. Depression as a result of chronic stress leads to anatomical and biochemical changes in cortical and subcortical structures of the brain, causing a disruption of the synthesis of serotonin and other neurotransmitters that affect not only the gastrointestinal tract, but the other functions of the autonomic nervous system. Reduced serotonergic and dopaminergic neurotransmission not only enhances inflammation, but, acting in tandem with the pro-inflammatory cytokines (eg, in systemic chronic infections) can lead to irreversible consequences, disrupting neuroplasticity and neuroregeneration. The article discusses the mechanisms of gut-brain axis pathology and the main targets for the treatment and rehabilitation: antidepressants, serotonin and norepinephrine agonists, nicotinic acetylcholine receptors.