Host Neuroendocrine Research Articles

Eating for 3.8 × 1013: Examining the Impact of Diet and Nutrition on the Microbiota-Gut-Brain Axis Through the Lens of Microbial Endocrinology.

The study of host-microbe neuroendocrine crosstalk, termed microbial endocrinology, suggests the impact of diet on host health and microbial viability is, in part, reliant upon nutritional modulation of shared host-microbe neuroendocrine axes. In the 1990's it was first recognized that neuroendocrine pathways are major components of the microbiota-gut-brain axis, and that diet-induced changes in the gut microbiota were correlated with changes in host behavior and cognition. A causative link, however, between nutritional-induced shifts in microbiota composition and change in host behavior has yet to be fully elucidated. Substrates found in food which are utilized by bacteria in the production of microbial-derived neurochemicals, which are structurally identical to those made by the host, likely represent a microbial endocrinology-based route by which the microbiota causally influence the host and microbial community dynamics via diet. For example, food safety is strongly impacted by the microbial production of biogenic amines. While microbial-produced tyramine found in cheese can elicit hypertensive crises, microorganisms which are common inhabitants of the human intestinal tract can convert L-histidine found in common foodstuffs to histamine and thereby precipitate allergic reactions. Hence, there is substantial evidence suggesting a microbial endocrinology-based role by which the gastrointestinal microbiota can utilize host dietary components to produce neuroactive molecules that causally impact the host. Conversely, little is known regarding the reverse scenario whereby nutrition-mediated changes in host neuroendocrine production affect microbial viability, composition, and/or function. Mechanisms in the direction of brain-to-gut, such as how host production of catecholamines drives diverse changes in microbial growth and functionality within the gut, require greater examination considering well-known nutritional effects on host stress physiology. As dietary intake mediates changes in host stress, such as the effects of caffeine on the hypothalamic-pituitary-adrenal axis, it is likely that nutrition can impact host neuroendocrine production to affect the microbiota. Likewise, the plasticity of the microbiota to changes in host diet has been hypothesized to drive microbial regulation of host food preference via a host-microbe feedback loop. This review will focus on food as concerns microbial endocrinology with emphasis given to nutrition as a mediator of host-microbe bi-directional neuroendocrine crosstalk and its impact on microbial viability and host health.

The Neuroendocrinology of the Microbiota-Gut-Brain Axis: A Behavioural Perspective.

The human gut harbours trillions of symbiotic bacteria that play a key role in programming different aspects of host physiology in health and disease. These intestinal microbes are also key components of the gut-brain axis, the bidirectional communication pathway between the gut and the central nervous system (CNS). In addition, the CNS is closely interconnected with the endocrine system to regulate many physiological processes. An expanding body of evidence is supporting the notion that gut microbiota modifications and/or manipulations may also play a crucial role in the manifestation of specific behavioural responses regulated by neuroendocrine pathways. In this review, we will focus on how the intestinal microorganisms interact with elements of the host neuroendocrine system to modify behaviours relevant to stress, eating behaviour, sexual behaviour, social behaviour, cognition and addiction.

Multidirectional chemical signalling between Mammalian hosts, resident microbiota, and invasive pathogens: neuroendocrine hormone-induced changes in bacterial gene expression.

Host-pathogen communication appears to be crucial in establishing the outcome of bacterial infections. There is increasing evidence to suggest that this communication can take place by bacterial pathogens sensing and subsequently responding to host neuroendocrine (NE) stress hormones. Bacterial pathogens have developed mechanisms allowing them to eavesdrop on these communication pathways within their hosts. These pathogens can use intercepted communication signals to adjust their fitness to persist and cause disease in their hosts. Recently, there have been numerous studies highlighting the ability of NE hormones to act as an environmental cue for pathogens, helping to steer their responses during host infection. Host NE hormone sensing can take place indirectly or directly via bacterial adrenergic receptors (BARs). The resulting changes in bacterial gene expression can be of strategic benefit to the pathogen. Furthermore, it is intriguing that not only can bacteria sense NE stress hormones but they are also able to produce key signalling molecules known as autoinducers. The rapid advances in our knowledge of the human microbiome, and its impact on health and disease highlights the potential importance of communication between the microbiota, pathogens and the host. It is indeed likely that the microbiota input significantly in the neuroendocrinological homeostasis of the host by catabolic, anabolic, and signalling processes. The arrival of unwanted guests, such as bacterial pathogens, clearly has a major impact on these delicately balanced interactions. Unravelling the pathways involved in interkingdom communication between invading bacterial pathogens, the resident microbiota, and hosts, may provide novel targets in our continuous search for new antimicrobials to control disease.

Pathogen espionage: multiple bacterial adrenergic sensors eavesdrop on host communication systems

The interactions between bacterial pathogens and their eukaryotic hosts are vital in determining the outcome of infections. Bacterial pathogens employ molecular sensors to detect and facilitate adaptation to changes in their niche. The sensing of these extracellular signals enables the pathogen to navigate within mammalian hosts. Intercellular bacterial communication is facilitated by the production and sensing of autoinducer (AI) molecules via quorum sensing. More recently, AI-3 and the host neuroendocrine (NE) hormones adrenaline and noradrenaline were reported to display cross-talk for the activation of the same signalling pathways. Remarkably, there is increasing evidence to suggest that enteric bacteria sense and respond to the host NE stress hormones adrenaline and noradrenaline to modulate virulence. These responses can be inhibited by α and β-adrenergic receptor antagonists implying a bacterial receptor-based sensing and signalling cascade. In Escherichia coli O157:H7 and Salmonella, QseC has been proposed as the adrenergic receptor. Strikingly, there is an increasing body of evidence that not all the bacterial adrenergic responses require signalling through QseC. Here we provide additional hypotheses to reconcile these observations implicating the existence of alternative adrenergic receptors including BasS, QseE and CpxA and their associated signalling cascades with major roles in interkingdom communication.

The host–parasite neuroimmunoendocrine network in schistosomiasis: consequences to the host and the parasite

The physiological interactions during the course of any immune response are complex. Infection induces antigen-specific recognition by the immune system, which is consequently charged with the responsibility of marshalling the appropriate effector responses necessary to destroy the pathogen, or at the very least inhibit its progression. Obviously, the immune system should accomplish this while minimizing collateral damage to the host or it risks, winning a Pyrrhic victory. As our understanding of the neuroendocrine system grows, it has become increasingly clear that this complex network of neurotransmitters, hormones and cytokines plays an important role in mediating immunity. Schistosomes present an especially complex relationship between pathogen and these physiological systems, with hormonally dependent host factors such as sex and age correlated with parasite success. In this report, we review the current literature on sex and age associations between infection and progression of disease. We then follow with a discussion on interactions between the host neuroendocrine and immune systems. We also speculate on strategies to apply this knowledge to novel treatment strategies. Results argue for a complex network comprising the immune, endocrinological and nervous systems of both host and schistosome in the regulation of the plural outcomes of infection.

Serum leptin levels in acute protein deprivation.

Protein energy malnutrition (PEM) induces a host neuroendocrine response, reflected by significant elevations in circulating glucocorticoid levels and associated with metabolic and immune dysfunction. Leptin regulates food intake and body mass and has a significant impact on the hypothalamic-pituitary-adrenal axis (HPA). We hypothesized that leptin may be altered by and may play an important role in regulating the effects of PEM. Female Balb/c mice were used. In experiment 1, mice were pair-fed either a protein-free (0% casein) or control (24% casein) diet for 7 days. In experiment 2, mice were implanted with either a placebo or corticosterone-releasing pellet and fed the control diet for 7 days. In experiment 3, adrenalectomized mice were pair-fed either the protein-free or control diet for 7 days. Serum corticosterone and leptin levels were measured in all experiments. PEM caused significant reductions in food intake, body weight, and total body fat, but not lean body mass. Serum corticosterone and leptin levels were significantly greater in mice fed the protein-free diet. Subcutaneous implantation of a corticosterone pellet in mice fed the control diet resulted in a significantly elevated serum leptin level compared with placebo-implanted controls. Bilateral adrenalectomy partially blunted the increased serum leptin in PEM. Leptin may be an important mediator of weight loss and decreased food intake in PEM. Elevated serum leptin in PEM may be secondary to elevated serum corticosterone, with other factors inherent in the host response to protein restriction also contributing to elevated serum leptin.

Mechanisms involved in parasitic castration: In vitro effects of the trematode Prosorhynchus squamatus on the gametogenesis and the nutrient storage metabolism of the marine bivalve mollusc Mytilus edulis

The mechanisms involved in the parasitic castration of the marine mussel Mytilus edulis by the trematode parasite Prosorhynchus squamatus Odhner, 1905, have been investigated in vitro with two bioassays employing dissociated host tissues. There is no conclusive evidence that P. squamatus affects the secretion of two host neuroendocrine factors, viz., gonial mitosis-stimulating factor and glycogen mobilization hormone, involved in the gametogenesis/nutrient storage cycles of the mussel. In contrast, extracts of P. squamatus sporocysts and cercariae significantly stimulated glycogen mobilization in host glycogen cells and strongly inhibited host gonial mitosis. A gonial mitosis-inhibiting factor (GMIF) was found in the hemolymph of parasitized mussels. The existence of an endogenous GMIF in mantle tissue of uninfected mussels has been demonstrated. This factor appeared to be secreted into the hemolymph during the period of sexual maturity. Whether the parasite acts directly on the host gonia, or by provoking the liberation of this endogenous GMIF, has yet to be ascertained. It would appear, however, that the parasite acts directly on host glycogen cells.