Microbiome and autoimmunity

In humans, most epithelial surfaces are colonized by complex ecosystem of microorganisms called microbiota. While each of these surfaces has unique microbial colony, host–microbe interactions are necessary for our adaptation to the environment, development of many physiological processes and their constant regulation. The largest microbial community resides in the gut, where it consists mainly of diverse community of bacteria, but fungi, protozoa, archaea and viruses (mostly bacteriophages) are present as well. Disruption of gut microbiota, i.e. dysbiosis, is associated with numerous inflammatory, metabolic, cardiovascular and neoplastic diseases. This extraordinarily broad scope of effects is caused either directly, by producing bioactive metabolites, or indirectly, by shaping the cellular and humoral response in the host's cells – mainly in the gut epithelial and immune cells, which can even reach distant organs and tissues. Dysbiosis is often associated with impaired barrier function (“leaky gut”) which leads increased interactions of the microbial antigens with the immune system and to local and systemic inflammation. Thus all actions influencing gut microbiota, such as shifts in diet, administration of antibiotics or probiotics or faecal microbiota transfer, have recently emerged as attractive therapeutic or preventive interventions in medicine. Here, I will shortly describe mechanisms of their action and outline concepts that bridge the gap between microbiota and immune mechanisms. Acknowledgement: Research is supported by Czech Academy of Sciences (Lumina Quaeruntur Program LQ200202105).