Live probiotic cultures and the gastrointestinal tract: symbiotic preservation of tolerance whilst attenuating pathogenicity.

Bacteria comprise the earliest form of independent life on this planet. Bacterial development has included co-operative symbiosis with plants (e.g., Leguminosae family and nitrogen fixing bacteria in soil) and animals (e.g., the gut microbiome). A fusion event of two prokaryotes evolutionarily gave rise to the eukaryote cell in which mitochondria may be envisaged as a genetically functional mosaic, a relic from one of the prokaryote cells. The discovery of bacterial inhibitors such chloramphenicol and others has been exploited to highlight mitochondria as arising from a bacterial progenitor. As such the evolution of human life has been complexly connected to bacterial activity. This is embodied, by the appearance of mitochondria in eukaryotes (alphaproteobacteria contribution), a significant endosymbiotic evolutionary event. During the twentieth century there was an increasing dependency on anti-microbials as mainline therapy against bacterial infections. It is only comparatively recently that the essential roles played by the gastrointestinal tract (GIT) microbiome in animal health and development has been recognized as opposed to the GIT microbiome being a toxic collection of micro-organisms. It is now well-documented that the GIT microbiome is comprised of a complex cohort of commensal and potentially pathogenic bacteria. Microbial interactions in the GIT provide the necessary cues for the development of regulated signals [in part by reactive oxygen species (ROS)] that promote immunological tolerance, metabolic regulation and stability, and other factors, which may then help control local and extra-intestinal end organ (e.g., kidneys) physiology. Pharmacobiotics, the administration of live probiotic cultures is an exciting growth area of potential therapeutics, developing together with an increased scientific understanding of GIT microbiome symbiosis in health and disease. Hence probiotic bacteria may provide a therapeutic connect with the GIT microbiome that can rescue mitochondrial dysfunction by linking a biologically plausible cellular signaling program (ROS reliant) between the human host and its microbiome cohort for a continued co-operative symbiosis that maintains homeostasis favorable to both.