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dc.contributor.authorIsaiah, Simon
dc.contributor.authorLoots, Du Toit
dc.contributor.authorMason, Shayne
dc.contributor.authorSolomons, Regan
dc.contributor.authorVan der Kuip, Martijn
dc.date.accessioned2020-05-14T13:17:21Z
dc.date.available2020-05-14T13:17:21Z
dc.date.issued2020
dc.identifier.citationIsaiah, S. et al. 2020. Overview of brain-to-gut axis exposed to chronic CNS bacterial infection(s) and a predictive urinary metabolic profile of a brain infected by mycobacterium tuberculosis. Frontiers in neuroscience, 14: #296. [https://doi.org/10.3389/fnins.2020.00296]en_US
dc.identifier.issn1662-4548
dc.identifier.issn1662-453X (Online)
dc.identifier.urihttp://hdl.handle.net/10394/34636
dc.identifier.urihttps://www.frontiersin.org/articles/10.3389/fnins.2020.00296/pdf
dc.identifier.urihttps://doi.org/10.3389/fnins.2020.00296
dc.description.abstractA new paradigm in neuroscience has recently emerged – the brain–gut axis (BGA). The contemporary focus in this paradigm has been gut → brain (“bottom-up”), in which the gut-microbiome, and its perturbations, affects one’s psychological state-of-mind and behavior, and is pivotal in neurodegenerative disorders. The emerging brain → gut (“top-down”) concept, the subject of this review, proposes that dysfunctional brain health can alter the gut-microbiome. Feedback of this alternative bidirectional highway subsequently aggravates the neurological pathology. This paradigm shift, however, focuses upon non-communicable neurological diseases (progressive neuroinflammation). What of infectious diseases, in which pathogenic bacteria penetrate the blood–brain barrier and interact with the brain, and what is this effect on the BGA in bacterial infection(s) that cause chronic neuroinflammation? Persistent immune activity in the CNS due to chronic neuroinflammation can lead to irreversible neurodegeneration and neuronal death. The properties of cerebrospinal fluid (CSF), such as immunological markers, are used to diagnose brain disorders. But what of metabolic markers for such purposes? If a BGA exists, then chronic CNS bacterial infection(s) should theoretically be reflected in the urine. The premise here is that chronic CNS bacterial infection(s) will affect the gut-microbiome and that perturbed metabolism in both the CNS and gut will release metabolites into the blood that are filtered (kidneys) and excreted in the urine. Here we assess the literature on the effects of chronic neuroinflammatory diseases on the gut-microbiome caused by bacterial infection(s) of the CNS, in the context of information attained via metabolomics-based studies of urine. Furthermore, we take a severe chronic neuroinflammatory infectious disease – tuberculous meningitis (TBM), caused by Mycobacterium tuberculosis, and examine three previously validated CSF immunological biomarkers – vascular endothelial growth factor, interferon-gamma and myeloperoxidase – in terms of the expected changes in normal brain metabolism. We then model the downstream metabolic effects expected, predicting pivotal altered metabolic pathways that would be reflected in the urinary profiles of TBM subjects. Our cascading metabolic model should be adjustable to account for other types of CNS bacterial infection(s) associated with chronic neuroinflammation, typically prevalent, and difficult to distinguish from TBM, in the resource-constrained settings of poor communitiesen_US
dc.language.isoenen_US
dc.publisherFrontiers Mediaen_US
dc.subjectGut-brain axisen_US
dc.subjectTuberculous meningitisen_US
dc.subjectImmunological biomarkeren_US
dc.subjectMetabolismen_US
dc.subjectUrinary profilingen_US
dc.subjectChronic neuroinflammationen_US
dc.subjectBacterial infectious diseasesen_US
dc.titleOverview of brain-to-gut axis exposed to chronic CNS bacterial infection(s) and a predictive urinary metabolic profile of a brain infected by mycobacterium tuberculosisen_US
dc.typeArticleen_US
dc.contributor.researchID10799508 - Loots, Du Toit
dc.contributor.researchID21487855 - Mason, Shayne William
dc.contributor.researchID26580748 - Isaiah, Simon


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