Abstract
ObjectiveTo examine whether maternal probiotic intervention influences the alterations in the brain-immune-gut axis induced by neonatal maternal separation (MS) and/or restraint stress in adulthood (AS) in Wistar rats.DesignDams had free access to drinking water supplemented with Bifidobacterium animalis subsp lactis BB-12® (3×109 CFU/mL) and Propionibacterium jensenii 702 (8.0×108 CFU/mL) from 10 days before conception until postnatal day (PND) 22 (weaning day), or to control ad lib water. Offspring were subjected to MS from PND 2 to 14 or left undisturbed. From PND 83 to 85, animals underwent 30 min/day AS, or were left undisturbed as controls. On PND 24 and 86, blood samples were collected for corticosterone, ACTH and IgA measurement. Colonic contents were analysed for the composition of microflora and luminal IgA levels.ResultsExposure to MS significantly increased ACTH levels and neonatal fecal counts of aerobic and anaerobic bacteria, E. coli, enterococci and clostridia, but reduced plasma IgA levels compared with non-MS animals. Animals exposed to AS exhibited significantly increased ACTH and corticosterone levels, decreased aerobic bacteria and bifidobacteria, and increased Bacteroides and E. coli counts compared to non-AS animals. MS coupled with AS induced significantly decreased anaerobes and clostridia compared with the non-stress adult controls. Maternal probiotic intervention significantly increased neonatal corticosterone levels which persisted until at least week 12 in females only, and also resulted in elevated adult ACTH levels and altered neonatal microflora comparable to that of MS. However, it improved plasma IgA responses, increased enterococci and clostridia in MS adults, increased luminal IgA levels, and restored anaerobes, bifidobacteria and E. coli to normal in adults.ConclusionMaternal probiotic intervention induced activation of neonatal stress pathways and an imbalance in gut microflora. Importantly however, it improved the immune environment of stressed animals and protected, in part, against stress-induced disturbances in adult gut microflora.
Highlights
Life stress has been reported to be associated with alterations to the development of the hypothalamic–pituitary– adrenal (HPA)-axis; a neuroendocrine system which is involved in the regulation of normal stress responses in vertebrates
Exposure to maternal separation (MS) significantly increased ACTH levels and neonatal fecal counts of aerobic and anaerobic bacteria, E. coli, enterococci and clostridia, but reduced plasma Immunoglobulin A (IgA) levels compared with non-MS animals
Animals exposed to adult restraint stress (AS) exhibited significantly increased ACTH and corticosterone levels, decreased aerobic bacteria and bifidobacteria, and increased Bacteroides and E. coli counts compared to non-AS animals
Summary
Life stress has been reported to be associated with alterations to the development of the hypothalamic–pituitary– adrenal (HPA)-axis; a neuroendocrine system which is involved in the regulation of normal stress responses in vertebrates. Early postnatal stress provokes dysregulations of HPA-axis function characterised by hyper-responsiveness to subsequent stress and long-term hyper-secretion of glucocorticoids [1]. This concept has been applied to the ontogeny of a variety of disorders later in life including functional gastro-intestinal disorders (FGIDs) such as irritable bowel syndrome (IBS) [2,3]. Neonatal maternal separation (MS) in rodents is a well-established model of human brain-gut axis alterations induced by early life trauma. MS resulted in gut dysfunctions such as increased mucosal ion transport [6,7,9] and epithelial permeability to macromolecules [6,7,8,9,10,11,12,13], increased mucosal adherent/penetrated commensal bacteria [6,7] and bacterial translocation to internal organs [13], decreased intestinal mucin/mucus [12,14], altered the integrity of gut microbiota [5,12,15], increased motility [9,16] and increased visceral/colonic sensitivity [5,11,16,17,18], induced intestinal morphological/structural damage and increased mucosal mast cells and goblet cells [11,13,14]
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