“We came up with the idea of testing a ketogenic diet… which in mice, it’s basically a lot of Crisco… giving a keto diet to mice with CGD… led to a decreased susceptibility to colitis.” —Dr. Emilia Liana Falcone
The microbiome isn’t something sitting on the sidelines. It’s part of the immune system, interacting with the barrier, shaping responses, and, in IEI, reflecting the underlying defect.
On this episode, Dr. Mariam Hanna is joined by Dr. Emilia Liana Falcone, physician-scientist and director of the Microbiome and Mucosal Defense Research Unit at the Montreal Clinical Research Institute, to walk through how these host–microbe interactions drive disease. From early-life immune programming to microbial signals that activate inflammatory pathways, this is a shift from association to mechanism. And a step toward therapies that target both sides of the equation.
Key Points:
The microbiome reflects the underlying immune defect in IEI
Focus on what microbes are doing, not just which ones are present
Microbiome changes both result from—and contribute to—disease
Early life is a critical window where these interactions are set
Loss of protective microbial functions matters more than specific bacteria
Microbial signals can directly drive inflammation (including inflammasome activation)
Future treatments will likely combine immune therapy with microbiome-targeted approaches
This is not about adding a probiotic.
It’s about understanding how immune defects reshape the microbial environment, and how that environment feeds back into disease.
Get that interaction right, and you’re not just managing symptoms.
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