Title:The Gut Microbiome
Volume: 13
Issue: 4
Author(s): Giovanni C. Actis
Affiliation:
Keywords:
Gut flora, gut microbiome, inflammasomes, inflammatory bowel disease, pathogen associated molecular patterns.
Abstract: Since the discovery and use of the microscope in the 17th century, we know that we host trillions of micro-organisms
mostly in the form of bacteria indwelling the “barrier organs” skin, gut, and airways. They exert regulatory functions, are in a
continuous dialogue with the intestinal epithelia, influence energy handling, produce nutrients, and may cause diabetes and
obesity. The human microbiome has developed by modulating or avoiding inflammatory responses; the host senses bacterial
presence through cell surface sensors (the Toll-like receptors) as well as by refining mucous barriers as passive defense
mechanisms. The cell density and composition of the microbiome are variable and multifactored. The way of delivery establishes
the type of initial flora; use of antibiotics is another factor; diet composition after weaning will shape the adult’s microbiome
composition, depending on the subject’s life-style. Short-chain fatty acids participate in the favoring action exerted by
microbiome in the pathogenesis of type-2 diabetes and obesity. Clinical observation has pinpointed a sharp rise of various
dysimmune conditions in the last decades, including IBD and rheumatoid arthritis, changes that outweigh the input of simple
heritability. It is nowadays proposed that the microbiome, incapable to keep up with the changes of our life-style and feeding
sources in the past few decades might have contributed to these immune imbalances, finding itself inadequate to handle the
changed gut environment. Another pathway to pathology is the rise of directly pathogenic phyla within a given microbiome:
growth of adherent E. coli, of C. concisus, and of C. jejuni, might be examples of causes of local enteropathy, whereas the genus
Prevotella copri is now suspected to be linked to rise of arthritic disorders. Inflammasomes are required to shape a non
colitogenic flora. Treatment of IBD and infectious enteritides by the use of fecal transplant is warranted by this knowledge.
