Adverse fluctuations in the distribution of the intestinal microbiome cohort has been associated with the onset of intra- and extra-intestinal inflammatory conditions, like the metabolic syndrome (MetS) and it's hepatic manifestation, non-alcoholic fatty liver disease (NAFLD). The intestinal microbial community of obese compared to lean subjects has been shown to undergo configurational shifts in various genera, including but not limited to increased abundances of Prevotella, Escherichia, Peptoniphilus, and Parabacteroides and decreased levels of Bifidobacteria, Roseburia, and Eubacteria genera. At the phylum level, decreased Bacteroidetes and increased Firmicutes have been reported. The intestinal microbiota therefore presents an important target for designing novel therapeutic modalities that target extra-intestinal inflammatory disorders, such as NAFLD. This review hypothesizes that disruption of the intestinal–mucosal macrophage interface is a key factor in intestinal-liver axis disturbances. Intestinal immune responses implicated in the manifestation, maintenance and progression of NAFLD provide insights into the dialogue between the intestinal microbiome, the epithelia and mucosal immunity. The pro-inflammatory activity and immune imbalances implicated in NAFLD pathophysiology are reported to stem from dysbiosis of the intestinal epithelia which can serve as a source of hepatoxic effects. We posit that the hepatotoxic consequences of intestinal dysbiosis are compounded through intestinal microbiota-mediated inflammation of the local mucosa that encourages mucosal immune dysfunction, thus contributing important plausible insight in NAFLD pathogenesis. The administration of probiotics and prebiotics as a cure-all remedy for all chronic diseases is not advocated, instead, the incorporation of evidence based probiotic/prebiotic formulations as adjunctive modalities may enhance lifestyle modification management strategies for the amelioration of NAFLD.

Immune defence against pathogenic agents comprises the basic premise for the administration of vaccines. Vaccinations have hence prevented millions of infectious illnesses, hospitalizations and mortality. Acquired immunity comprises antibody and cell mediated responses and is characterized by its specificity and memory. Along a similar congruent yet diverse mode of disease prevention, the human host has negotiated from in utero and at birth with the intestinal commensal bacterial cohort to maintain local homeostasis in order to achieve immunological tolerance in the new born. The advent of the Human Microbiome Project has redefined an appreciation of the interactions between the host and bacteria in the intestines from one of a collection of toxic waste to one of a symbiotic existence. Probiotics comprise bacterial genera thought to provide a health benefit to the host. The intestinal microbiota has profound effects on local and extra-intestinal end organ physiology. As such, we further posit that the adjuvant administration of dedicated probiotic formulations can encourage the intestinal commensal cohort to beneficially participate in the intestinal microbiome-intestinal epithelia-innate-cell mediated immunity axes and cell mediated cellular immunity with vaccines aimed at preventing infectious diseases whilst conserving immunological tolerance. The strength of evidence for the positive effect of probiotic administration on acquired immune responses has come from various studies with viral and bacterial vaccines. We posit that the introduction early of probiotics may provide significant beneficial immune outcomes in neonates prior to commencing a vaccination schedule or in elderly adults prior to the administration of vaccinations against influenza viruses.

The interactions of micro-organisms cohabitating with Homo sapiens spans millennia, with microbial communities living in a symbiotic relationship with the host. Interacting to regulate and maintain physiological functions and immunological tolerance, the microbial community is able to exert an influence on host health. An example of micro-organisms contributing to an intestinal disease state is exhibited by a biodiverse range of protozoan and bacterial species that damage the intestinal epithelia and are therefore implicated in the symptoms of diarrhea. As a contentious exemplar, Blastocystis hominis is a ubiquitous enteric protist that can adversely affect the intestines. The symptoms experienced are a consequence of the responses of the innate immune system triggered by the disruption of the intestinal barrier. The infiltration of the intestinal epithelial barrier involves a host of immune receptors, including toll like receptors and IgM/IgG/IgA antibodies as well as CD8+ T cells, macrophages, and neutrophils. Whilst the mechanisms of interactions between the intestinal microbiome and protozoan parasites remain incompletely understood, it is acknowledged that the intestinal microbiota is a key factor in the pathophysiology of parasitic infections. Modulating the intestinal environment through the administration of probiotics has been postulated as a possible therapeutic agent to control the proliferation of intestinal microbes through their capacity to induce competition for occupation of a common biotype. The ultimate goal of this mechanism is to prevent infections of the like of giardiasis and eliminate its symptoms. The differing types of probiotics (i.e., bacteria and yeast) modulate immunity by stimulating the host immune system. Early animal studies support the potential benefits of probiotic administration to prevent intestinal infections, with human clinical studies showing probiotics can reduce the number of parasites and the severity of symptoms. The early clinical indications endorse probiotics as adjuncts in the pharmaceutical treatment of protozoan infections. Currently, the bar is set low for the conduct of well-designed clinical studies that will translate the use of probiotics to ameliorate protozoan infections, therefore the requisite is for further clinical research.

The authors wish to make the following corrections to this paper due to a typesetting error in the conclusion of this article which was recently published in Vaccines[...]