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Role of probiotics in correcting abnormalities of colonic flora induced by stress
  1. Helene Eutamene,
  2. Lionel Bueno
  1. Neuro-Gastroenterology and Nutrition Unit, Toulouse, France
  1. Dr H Eutamene, Neuro-Gastroenterology and Nutrition Unit, 180 Chemin de Tournefeuille, BP3, 31931 Toulouse Cedex; France; heutamen{at}toulouse.inra.fr

https://doi.org/10.1136/gut.2007.124040

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    Probiotics organise gut microflora for better regulation of the HPA axis not only in the early years but also during adulthood

    It is suggested that daily environmental and emotional stressful life events contribute to the development and reactivation of intestinal inflammation in chronic inflammatory bowel disease (IBD), to the clinical manifestations of irritable bowel syndrome (IBS) and to the development of food allergies by sensitisation of intestinal tissue to oral antigens through an increase of transepithelial permeability and luminal antigen uptake.1–3 In animal models of IBD, stress increases the severity of colitis and lowers the threshold for reactivation of mucosal inflammation.4 Stressful stimuli are known to affect gastrointestinal functions such as gut motility and secretion, and to increase paracelullar permeability. Defective epithelial barrier function, which can be measured as increased intestinal permeability, has been implicated in IBS and in IBD, in which it can predict relapse during clinical remission.5 6 In animal models, both acute (partial restraint stress) and chronic (neonatal) stress enhance luminal bacterial adherence and internalisation,7 increase bacterial translocation8 and activate immune reactions within the gut resulting from alterations in gut paracellular permeability.9 Recently, it was also shown that acute stress-induced hypersensitivity to distension results from an alteration of colonic paracellular permeability.10

    PROBIOTICS CORRECTING GUT MICROBIOTA AND GUT PERMEABILITY DISTURBANCES INDUCED BY STRESS

    Figure 1 (points 1 and 2) illustrates the following reactions.

    Figure 1 Proposed pathways for the correction by probiotics of abnormalities of colonic flora induced by stress. Published reports provide evidence for a potential use of probiotics in gastrointestinal disorders such as inflammatory bowel disease, inflammatory bowel syndrome and food allergies. Stressful life events contribute to the development of these diseases accompanied with gastrointestinal function alterations. Probiotics can correct gut disturbances induced by stress by targeting several sites of action, resulting in a long gut–brain neuroimmune reflex pathway. (1) Locally, at the epithelium site, probiotics have numerous properties—namely, a trophic effect on intestinal villosities, normalisation of gut microbiota, prevention of adhesion of luminal bacteria, and reinforcement of the barrier function by enhancing barrier integrity. (2) At the intestinal mucosal level, probiotics by secretion of soluble factors or directly through activation of specific receptors, such as Toll-like receptors (TLRs), mannose receptors or dendritic cell-specific intercellular adhesion molecule 3-grabbing nonintegrin (DC-SIGN) from dendritic cells (DCs) can stimulate other immune cells like mast cells, T lymphocytes, normalising the ratio of pro- versus anti-inflammatory cytokines. (3) Through a cytokine neurohumoral route, probiotics may indirectly stimulate afferent nerve fibres—that is, vagus afferents, resulting in (4) a reduction in the levels of systemic corticosterone and adrenocorticotrophic hormone (ACTH).

    Numerous abnormalities of the gut flora have been described in patients with IBD and IBS. The presence of bacterial overgrowth in some patients with IBS and the improvement of their symptoms by oral antibiotics illustrate an enteric microbiota involvement in the genesis of the disease.11 12 Recent data support a potential role of probiotics for in alleviating IBS symptoms and suggest that the effects are strain-dependent. For example, a dietary administration of Lactobacillus plantarum 299 V …

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    • Conflict of interest: None.