The role of intestinal microbiota in the pathophysiology of depression

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Abstract

Depression is a mental disorder with a high prevalence. According to World Health Organization, it is a frequent cause of disability and the leading cause of suicide, with its risk increasing with age. The disorder is commonly diagnosed in patients with acute or chronic inflammatory conditions. Depression is typically accompanied by weakened T cell-mediated immunity, as well as abnormal secretion of pro- and anti-inflammatory cytokines and the resulting imbalance between them. The current developments in the field include a link established between depression and changes in intestinal microflora, suggested by numerous trials involving animals and also a small number of studies conducted on people. This paper is a review of the publications regarding the role of intestinal microbiota in the pathophysiology of depression found in PubMed and Web of Science repositories. The results of studies published over the last decade confirm the significance of intestinal microbiota for the pathophysiology of depression. One of the ways in which intestinal microbiota may impact the development of depression is the response of the innate immunity system to bacterial lipopolysaccharide (LPS), resulting with the stimulation of pro-inflammatory cytokines. The modifications of gut microflora have also been linked to changes in the hypothalamic- pituitary-adrenal axis, in the metabolism of tryptophan, (which is a serotonin substrate) and in neurotransmitter levels in the brain. Even though the results cited in this review seem promising, our current state of knowledge in this respect remains far from satisfactory, warranting further investigation into the potential of bacteria for supplementing the pharmacological therapy of depression.

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Stefaniak, A., Janion, K., & Stanuch, B. (2018). The role of intestinal microbiota in the pathophysiology of depression. Postepy Higieny i Medycyny Doswiadczalnej. Polska Akademia Nauk. https://doi.org/10.5604/01.3001.0012.4676

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