Microbial endocrinology: host–bacteria communication within the gut microbiome

Sandrini, Sara M.; Aldriwesh, Marwah; Alruways, Mashael W.l; Freestone, Primrose

doi:10.1530/joe-14-0615

Cited by 111 publications

(89 citation statements)

References 104 publications

(168 reference statements)

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“…Host hormonal signals are able to shape the behaviour of the gut microbiome, and in return, the microbiome residents signal the changes to their host and can affect physical and even mental well-being. 50 For example, endogenous hormones such as catecholamines enhance bacterial adhesion of pathogens to the host tissues 51 or downregulate resistance of pathogens of host microbial peptides. 52 Another study has shown that the human sex hormones decrease bacterial virulence by inhibiting quorum sensing, which is a specific communication between the bacterial and neuroendocrine systems.…”

Section: Discussionmentioning

confidence: 99%

Bifidobacterium longum and Lactobacillus helveticus Synergistically Suppress Stress-related Visceral Hypersensitivity Through Hypothalamic-Pituitary-Adrenal Axis Modulation

Ait-Belgnaoui

Payard

Rolland

et al. 2018

J Neurogastroenterol Motil

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Background/AimsVisceral pain and hypothalamic-pituitary-adrenal axis (HPA) dysregulation is a common characteristic in irritable bowel syndrome (IBS) patients. Previously, we reported that a probiotic formulation (Lactobacillus helveticus R0052 and Bifidobacterium longum R0175) prevents chronic stress-mediated brain function abnormalities by attenuating the HPA axis response. Here, we compared the effect between different probiotic treatments on the perception of visceral pain during colorectal distension (CRD) following a chronic stress and the consequences to the activity of the HPA axis. MethodsAfter a 2-week treatment with a combined probiotic formulation, or L. helveticus or B. longum alone in stressed mice, the visceral pain in response to CRD was recorded. The expression of glucocorticoid receptors was determined in the different brain areas involved in the stress response (hypothalamus, hippocampus, and prefrontal cortex). The plasma levels of stress hormones were also measured. ResultsA pretreatment using the combination of probiotic formulation significantly reduces the chronic stress-induced visceral hypersensitivity respectively at 0.06, 0.08, and 0.10 mL CRD volume. However, a single probiotic (B. longum or L. helveticus) administration is less effective in reducing visceral pain in stressed mice. Moreover, the expression of the glucocorticoid receptor mRNA was consistently up-regulated in several brain areas after pretreatment with a combined probiotic, which correlated with the normalization of stress response compared to the inconsistent effects of a single probiotic. ConclusionThe combination of L. helveticus and B. longum is more effective in regulating glucocorticoid negative feedback on the HPA axis than probiotic alone and subsequently in treating stress-induced visceral pain.

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Section: Discussionmentioning

confidence: 99%

Bifidobacterium longum and Lactobacillus helveticus Synergistically Suppress Stress-related Visceral Hypersensitivity Through Hypothalamic-Pituitary-Adrenal Axis Modulation

Ait-Belgnaoui

Payard

Rolland

et al. 2018

J Neurogastroenterol Motil

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“…118,119 In vitro, the growth of P aeruginosa is increased by the presence of catecholamines (figure 4). 51 In human bronchoalveolar lavage samples, increased alveolar catecholamine concentrations correlate strongly with collapse of the lung microbiome around one dominant species (most frequently P aeruginosa , figure 4).…”

Section: The Radically Altered Ecology Of the Injured Alveolusmentioning

confidence: 99%

The microbiome and critical illness

Dickson

2016

The Lancet Respiratory Medicine

355

344

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The central role of the microbiome in critical illness is supported by a half century of experimental and clinical study. The physiological effects of critical illness and the clinical interventions of intensive care substantially alter the microbiome. In turn, the microbiome predicts patients’ susceptibility to disease, and manipulation of the microbiome has prevented or modulated critical illness in animal models and clinical trials. This Review surveys the microbial ecology of critically ill patients, presents the facts and unanswered questions surrounding gut-derived sepsis, and explores the radically altered ecosystem of the injured alveolus. The revolution in culture-independent microbiology has provided the tools needed to target the microbiome rationally for the prevention and treatment of critical illness, holding great promise to improve the acute and chronic outcomes of the critically ill.

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“…Moreover, evidence that levels of biologically active CAs in the intestinal lumen require specific bacterial-encoded enzymes suggests that luminal CA levels are gut microbiota-dependent (28). CAs continue to attract interest as communication molecules between host cells and microbes; these stress signals may influence microbial dysbiosis and increase the susceptibility to infection by altering the growth and virulence of human pathogens, including Enterobacteriaceae species (29,30).…”

mentioning

confidence: 99%

QseC inhibition as an antivirulence approach for colitis-associated bacteria

Rooks

Veiga

Reeves

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Hosts and their microbes have established a sophisticated communication system over many millennia. Within mammalian hosts, this dynamic cross-talk is essential for maintaining intestinal homeostasis. In a genetically susceptible host, dysbiosis of the gut microbiome and dysregulated immune responses are central to the development of inflammatory bowel disease (IBD). Previous surveys of stool from the T-bet −/− Rag2 −/− IBD mouse model revealed microbial features that discriminate between health and disease states. Enterobacteriaceae expansion and increased gene abundances for benzoate degradation, two-component systems, and bacterial motility proteins pointed to the potential involvement of a catecholamine-mediated bacterial signaling axis in colitis pathogenesis. Enterobacteriaceae sense and respond to microbiota-generated signals and host-derived catecholamines through the two-component quorum-sensing Escherichia coli regulators B and C (QseBC) system. On signal detection, QseC activates a cascade to induce virulence gene expression. Although a single pathogen has not been identified as a causative agent in IBD, adherent-invasive Escherichia coli (AIEC) have been implicated. Flagellar expression is necessary for the IBD-associated AIEC strain LF82 to establish colonization. Thus, we hypothesized that qseC inactivation could reduce LF82's virulence, and found that an absence of qseC leads to down-regulated flagellar expression and motility in vitro and reduced colonization in vivo. We extend these findings on the potential of QseC-based IBD therapeutics to three preclinical IBD models, wherein we observe that QseC blockade can effectively modulate colitogenic microbiotas to reduce intestinal inflammation. Collectively, our data support a role for QseC-mediated bacterial signaling in IBD pathogenesis and indicate that QseC inhibition may be a useful microbiota-targeted approach for disease management.colitis | Escherichia coli | QseC | antivirulence | gut microbiome

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Microbial endocrinology: host–bacteria communication within the gut microbiome

Cited by 111 publications

References 104 publications

Bifidobacterium longum and Lactobacillus helveticus Synergistically Suppress Stress-related Visceral Hypersensitivity Through Hypothalamic-Pituitary-Adrenal Axis Modulation

Bifidobacterium longum and Lactobacillus helveticus Synergistically Suppress Stress-related Visceral Hypersensitivity Through Hypothalamic-Pituitary-Adrenal Axis Modulation

The microbiome and critical illness

QseC inhibition as an antivirulence approach for colitis-associated bacteria

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