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Dr. Odufalu:
Hello. My name is Dr. Florence-Damilola Odufalu. I am a gastroenterologist at Keck School of Medicine of USC.

The gut microbiome plays a central role in IBD pathophysiology by maintaining intestinal homeostasis through barrier support, immune regulation, and metabolite production, but dysbiosis disrupts this balance to promote chronic inflammation.

Dysbiosis is characterized by reduced microbial diversity and a loss of beneficial taxa, resulting in decreased production of protective metabolites such as butyrate. A loss of short-chain fatty acids weakens the epithelial barrier, while expansion of proinflammatory microbes leads to mucus degradation, mucosal invasion, and Th17 interleukin-17 activation.

Altered microbial metabolites shift immune signaling toward proinflammatory pathways. For example, nuclear factor kappa beta, interleukin-23 and Th17.

Barrier disruption and metabolite loss increase intestinal permeability, triggering innate immune activation, including the NOD2 and PAMP pathways. Together, these changes disrupt the Treg–Th17 balance, promoting chronic intestinal inflammation, particularly in genetically susceptible individuals.

As you can see in this image here in healthy gut mucosa, you see that there is an intact mucous membrane as well as an intact epithelial border. However, when you start to see different factors—and that could be from lifestyle and dietary factors, environmental triggers, or genetic drivers—that change this barrier, you can see that prior to the disease becoming fully chronic and inflammatory, you see that the immune system is activated, the commensal population of good and healthy bacteria start to decrease, and there is an emergence of those bad bacteria, which leads to the compromised barrier function.

Once you get a break in that mucosal barrier, you start to activate the inflammatory cascade and there is increase in pathobionts and then there's a loss of that beneficial microbes as well as a predominance of these microbes that lead to and trigger chronic inflammation. Once this sets in, you have uncontrolled and persistent inflammation that leads to an inability to shut down the activated immune response, triggering an immune imbalance.

There are several misconceptions and myths about the microbiome and what triggers and what quiets disease. We have a lot of discussions in my clinic about microbiome probiotics; however, the data is not completely out there and randomized data to support the use of probiotics in preventing and in treating inflammation.

However, there's one caveat, and that is in pouchitis. We have good data to support that antibiotics can help to improve pouchitis symptoms and there are some probiotics that can help to reduce recurring flares of chronic pouchitis.

Placing a focus on the gut microbiome isn't just a passing fad, it's central to the IBD story from risk all the way to remission. As our tools improve, so will our ability to personalize care around it. Thanks to everyone for joining me.

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