Gene expression of antimicrobial peptides in rat intestine under conditions of chronic stress

BACKGROUND: Severe stress causes an array of dysfunctions in the immune, neuroendocrine, cardiovascular, digestive and other systems, resulting in an emergence of various types of pathology. Common manifestations of a chronic stress are the disorders in the gastrointestinal tract, such as irritable bowel syndrome, functional dyspepsia, biliary dyskinesia, dysbiosis, inflammatory processes that determine the development of gastritis and one of the most widespread post-stress pathologies of the gastrointestinal tract — stomach ulcers. The disclosure of the molecular mechanisms of a pathogenesis of diseases associated with gastrointestinal dysfunction related to chronic stress as well as a search for new ways to correct these disorders are important tasks of fundamental and clinical medicine. The present work is focused on evaluating a participation of molecular factors of the innate immunity in intestine, such as antimicrobial peptides secreted by intestinal epithelial cells upon infection, in a response to the chronic stress. AIM: The aim of the study was to estimate the gene expression of a number of antimicrobial peptides: intestinal α- and β-defensins of laboratory animals (rats) under chronic stress conditions. MATERIALS AND METHODS: Modeling of a chronic stress was performed by daily forced swimming of laboratory animals in cold water. An expression of α- and β-defensin genes was evaluated using a real-time polymerase chain reaction. RESULTS: We found an increase in the level of expression of the rat α-defensin-5 and β-defensin-3 genes in response to chronic stress, while the expression of β-defensin-2 gene was not changed compared to the control. CONCLUSIONS: Considering that changes in the concentration and spectrum of peptides with antibacterial activity, caused by prolonged stress, can contribute to modification of the composition of the intestinal microbiota, the data obtained can expand our understanding of the molecular basis of the pathogenesis of diseases associated with disorders in the composition of microbiota under stress.