The gastro-intestinal tract is an ecosystem containing trillions of commensal bacteria living in symbiosis with the host. These microbiota modulate a variety of our physiological processes, including production of vitamins, absorption of nutrients and development of the immune system. One of their major functions is to fortify the intestinal barrier, thereby helping to prevent pathogens and harmful substances from crossing into the general circulation. Recently, effects of these microbiota on other blood-tissue barriers have also been reported. Here, we review the evidence indicating that gut bacteria play a role in regulating the blood-brain and blood-testis barriers. The underlying mechanisms include control of the expression of tight junction proteins by fermentation products such as butyrate, which also influences the activity of histone deacetylase.

In recent years, it has become clear that microbiome play a variety of essential roles in human metabolism, immunity, and overall health and that the composition of these microbiome is influenced by our environment, diet, weight, hormones, and other factors. Indeed, numerous physiological and pathological conditions, including obesity and metabolic syndrome, are associated with changes in our microbiome, referred to as dysbiosis. As a result, it is not surprising that such changes occur during pregnancy, which includes substantial weight gain and significant changes in metabolism and immune defenses. The present review relates physiological changes during pregnancy to alterations in the microbial composition at various sites, including the gut, oral cavity, and vagina. Pregnancy has been linked to such microbial changes, and we believe that, in contrast to certain disease states, these microbial changes are vital for a healthy pregnancy, probably through their influence on the mother’s immunological, endocrinological, and metabolic status.

Over the past decade, the scientific committee has called for broadening our horizons in understanding host–microbe interactions and infectious disease progression. Owing to the fact that the human gut harbors trillions of microbes that exhibit various roles including the production of vitamins, absorption of nutrients, pathogen displacement, and development of the host immune system, particular attention has been given to the use of germ-free (GF) animal models in unraveling the effect of the gut microbiota on the physiology and pathophysiology of the host. In this review, we discuss common methods used to generate GF fruit fly, zebrafish, and mice model systems and highlight the use of these GF model organisms in addressing the role of gut-microbiota in gut-related disorders (metabolic diseases, inflammatory bowel disease, and cancer), and in activating host defense mechanisms and amending pathogenic virulence.

By the beginning of 2020, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has rapidly evolved into an emergent worldwide pandemic, an outbreak whose unprecedented consequences highlighted the existing flaws within the global public healthcare systems. While the coronavirus disease 2019 (COVID-19) is bestowed with a broad spectrum of clinical manifestation involving vital organs, the respiratory system transpires as the main route of entry of SARS-CoV-2, with the lungs being its primary target. Of those infected, up to 20% require hospitalization on account of severity, while the majority of patients are either asymptomatic or exhibit mild symptoms. Exacerbation in disease severity and complications of COVID-19 infection have been allied with multiple comorbidities including hypertension, diabetes mellitus, cardiovascular disorders, cancer, and chronic lung disease. Interestingly, a recent body of evidence have foregrounded the pulmonary and gut microbiome as potential modulators in altering the course of COVID-19, plausibly via the microbiome-immune system axis. While relative concordance between microbes and immunity is still not fully elucidated in a COVID-19 disease context, we present here an overview of our current understanding of this COVID-19-microbiome-immune cross talk and discuss the potential contributions of microbiome-related immunity to SARS-CoV-2 pathogenesis and COVID-19 disease progression.

Chronic kidney disease (CKD) may be fatal for its victims and is an important long-term public health problem. The complicated medical procedures and diet restrictions to which patients with CKD are subjected alter the gut microbiome in an adverse manner, favoring over-accumulation of proteolytic bacteria that produce ammonia and other toxic substances. The present study aimed to investigate the effect of GA on 1) the composition of the gut microbiome and 2) on plasma levels of short-chain fatty acids. Male Wister rats were divided into four groups (six each) and treated for 4 weeks based on the following: control, dietary adenine (0.75%, w/w) to induce CKD, GA in the drinking water (15%, w/v), and both adenine and GA. At the end of the treatment period, plasma, urine, and fecal samples were collected for determination of several biochemical indicators of renal function and plasma levels of short-chain fatty acids (SCFAs) as well as characterization of the gut microbiome. Dietary adenine induced the typical signs of CKD, i.e., loss of body weight and impairment of renal function, while GA alleviated these effects. The intestine of the rats with CKD contained an elevated abundance of pathogenic Proteobacteria, Actinobacteria, and Verrucomicrobia but lowered proportions of Lactobacillaceae belonging to the Firmicutes phylum. Plasma levels of propionate and butyrate were lowered by dietary adenine and restored by GA. A negative association (Spearman’s p-value ≤ 0.01, r ≤ 0.5) was observed between Firmicutes and plasma creatinine, urea, urine N-acetyl-beta-D-glucosaminidase (NAG) and albumin. Phylum Proteobacteria on the other hand was positively associated with these markers while Phylum Bacteroidetes was positively associated with plasma SCFAs. In conclusion, the adverse changes in the composition of the gut microbiome, plasma levels of SCFAs, and biochemical indicators of renal function observed in the rats with CKD induced by dietary adenine were mitigated by GA. These findings are indicative of a link between uremia and the composition of the microbiome in connection with this disease. Dietary administration of GA to patients with CKD may improve their renal function via modulating the composition of their microbiome—a finding that certainly warrants further investigation.