Table 2.
Psychiatric Disorder | Impact on Microbiota | References |
---|---|---|
Schizophrenia | Increased immune activation against dietary proteins and pathogens and continuous exposure to antigens predisposing the digestive system to chronic inflammation; alteration of permeability of the intestinal blood barrier and an increased risk of passage into the systemic circulation of bacterial and food peptides; increased inflammatory state with production of pro-inflammatory cytokines. | Caso et al., 2016 [44] |
Stimulation of Th17 cells in response to external stimuli, with consequent gastrointestinal inflammation causing intestinal dysbiosis. Maternal infections during pregnancy inducing a pro-inflammatory activation state responsible of metabolic consequences in the long period (reduced glycemic regulation, insulin resistance, increased body weight). Association of schizophrenia with irritable bowel syndrome influenced by gut microbiota, through bacterial translocation. |
Torrey et al., 2012 [50] Labouesse et al., 2015 [52] Severance et al., 2016 [55] |
|
Bipolar Disorder | Lower proportion of Faecalibacterium corresponding to a worsening of the pathology. | Painold et al., 2017 [66] |
Greater representation of the phylum Actinobacteria, with higher concentration of Prevotella and Enterobacter species, and gram-positive bacteria Atopobium Cluster, Clostridium, Flavinofractor. Prevotella more represented in bipolar type 1 patients, while Collinsella more abundant in bipolar type 2 patients. Production of neuroactive kynurenine, capable of inhibit the synthesis of 5-HT and interfere with the secretion of dopamine and GABA. Synaptic pruning could be modified by a direct effect of gut microbiota on microglial cells, especially in the ventral prefrontal and limbic cortex. |
Gondalia et al., 2019 [69] Lucidi et al. 2021 [68] Schwarcz et al., 2017 [33] Strakowski et al., 2012 [72] |
|
Unipolar Affective Disorder | Intestinal bacteria can change function of the hypotalamic–pituitary–andrenal axis (HPA) leading to an increased concentration of cortisol and pro-inflammatory molecules: the proinflammatory state increases the intestinal barrier permeability, facilitating the access to the bloodstream for gram-negative bacteria and inducing chronic inflammation in the central nervous system. The possible microbial profile in depressed patients can be defined by a reduction in the concentration of Firmicutes, Bacteroides and Proteobacteria, or by increased levels of Actinobacteria and Fusobacteria, Prevotellaceae and Lachnospiraceae. |
Li et al., 2019 [91] Barandouzi et al., 2020 [93] |
Decreased concentrations of Bifidobacterium, Firmicutes, Lactobacillus, Faecalibacterium and Ruminococcus and increased concentrations of Proteobacteria, Bacteroides and Prevotella in the gut microbiota of depressed patients. | Liu et al., 2016 [97] | |
Anxiety Disorders | Stressful events during intrauterine life and early childhood are associated with intestinal dysbiosis in the unborn child and in the mother. Alterations in the microbiota associated with increased concentrations of circulating corticosterone in response to stressful events, with transmission of stressed-altered maternal microbiota have long-term effects on gene expression at level of the hypothalamic paraventricular nucleus. The microbiota could regulate the serotonin system in the brain, influencing the hypotalamic–pituitary–andrenal axis and modifying gene expression at hippocampal and hypothalamic levels. |
Jašarević et al., 2021 [131] Neufeld et al., 2011 [142] |
Anorexia Nervosa | Increased concentration of bacteria of the species Clostridia, Enterobacteriaceae and M. Smithii and reduction in the species Roseburia. The intestinal microbiota transforms the proceeds of the diet into a large variety of products including vitamins, amino acid derivatives and short-chain fatty acids, able to modulate the permeability of the blood–brain barrier. |
Roubalová et al., 2020 [151] Parker et al., 2020 [167] |
Bulimia Nervosa | Increased levels of caseinolytic proteinase B, produced by E. Coli, which in turn stimulate autoimmunity response. The activity of the centers of appetite is complexly regulated by an elaborate neuroimmunoendocrine communication system, with the microbiota regulating the activity of adipose tissue and general homeostasis. |
Smitka et al., 2021 [154] Lucas et al., 2019 [156] |