Hi I'm Andrew Gewirtz from
Georgia State University's Center for Inflammation Immunity and Infection.
My presentation is entitled Gut Microbiota Chronic Inflammation and Metabolic Syndrome.
This illustration is an artist's rendition of the intestinal microbiota,
designed to show the great diversity that exists in this complex ecosystem.
This is a photograph of the intestinal mucosa
showing the population of 100 trillion bacteria,
50 percent of the lumenal contents by weight,
that live in close proximity to the intestinal epithelium.
This population of bacteria is quite diverse,
comprised of over 5000 distinct species and 2 million distinct genes.
These bacteria are a functional continuum with
some being mutualistic and that they benefit the host,
a few being pathogenic and that they can cause disease.
But the vast majority being somewhere in between either commensal or opportunists.
These bacteria are inhabiting a large area,
specifically the surface area of the intestine is approximately that of a tennis court.
Unlike the skin, which is essentially a closed barrier,
the intestines should be thought of as an active port.
The microbiota is acquired or inherited early in life and once
its composition is stable it tends to remain that way over the lifetime of the host.
The microbiota is essential for immune development and metabolic health,
but has also been linked to a variety of
chronic inflammatory diseases in the gut and beyond.
Thus, it's reasonable to think of
the enteric microbiota as your BFF or Best Frenemy Forever.
In that context, a goal of the Mucosal Immune system
is to expediently detect and clear pathogens,
while keeping opportunists in check.
This must be done while avoiding harm to beneficial microbes and host tissues.
This is analogous to managing a large bustling metropolis.
The overall message of this talk is that,
poorly managed gut microbiota can result in multiple flavors of gut inflammation,
including inflammatory bowel disease and metabolic syndrome.
This slide is a simplified schematic of the function of Toll-like receptors,