Abstract
The gastro-intestinal tract hosts a complex microbial ecosystem, the gut microbiota, whose collective genome coding capacity exceeds that of the host genome. The gut microbiota is nowadays regarded as a full organ, likely to contribute to the development of pathologies when its dynamic balance is disrupted (dysbiosis). In the last decade, evidence emerged that the gut microbiota influences brain development and function. In particular, comparisons between germ-free and conventional laboratory rodents showed that the absence of the gut microbiota exacerbates the hypothalamic pituitary adrenal (HPA) system reactivity to stress and alters the anxiety-like behaviour. Furthermore, the dysfunctions observed in germ-free animals can be corrected if the gut microbiota is restored in early life but not in adulthood, suggesting a critical period for microbiota imprinting on the responsiveness to stress. The modes of action are still to be deciphered. They may involve transport of neuroactive bacterial metabolites to the brain through the bloodstream, stimulation of the vagus nerve or of entero-endocrine cells, or modulation of the immune system and, consequently, of the inflammatory status. The discovery that the gut microbiota regulates the neuroendocrine and behavioural responses to stress paves the way for the hypothesis that gut microbiota dysbioses could contribute to the pathophysiology of anxiety-related disorders. In this regard, treatments of anxiety-prone rodent strains with probiotics or antibiotics aimed at modifying their gut microbiota have shown an anxiolytic-like activity. Clinical trials are now needed to know if results obtained in preclinical studies can translate to humans.
Highlights
The gastro-intestinal tract is inhabited with 1014 bacterial cells, a figure ten times greater than the total of eukaryotic cells in the human body
The great advances made in the last fifteen years in culture-independent techniques, including quantitative PCR, fluorescent in situ hybridization (FISH), genetic fingerprinting and sequencing based methods have revolutionized our knowledge of the taxonomic diversity, community structure and metabolic capability of the gut microbiota (Delzenne et al, 2011; Grenham et al, 2011; Lozupone et al, 2012; Weinstock, 2012)
This observation indicates that the physiological characteristics, habitats and diet exert a key influence on the gut microbiota community structure but the underlying mechanisms remain to be identified
Summary
The gastro-intestinal tract is inhabited with 1014 bacterial cells, a figure ten times greater than the total of eukaryotic cells in the human body. The infant gut microbiota is vulnerable and factors such as the delivery mode, breastfeeding vs bottle-feeding or antibiotic treatments may influence the colonization, and the community structure and functional capabilities of the gut microbiota in later life (Campeotto et al, 2007; Delzenne et al, 2011; Favier et al, 2002; Grenham et al, 2011; Lozupone et al, 2012). Other experiments with Swiss mice showed an increase of the baseline serum corticosterone concentration in GF animals compared with conventional counterparts (Gareau et al, 2011; Neufeld et al, 2011) Overall, all these studies show that the absence of the gut microbiota fundamentally intensifies the HPA axis activity (Fig. 2)
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