Jessica R. Allegretti, MD, MPH and Zain Kassam, MD, MPH
For many years, peptic ulcers were thought to be related to stress and lifestyle factors. Dr. Barry Marshall and Dr. Robin Warren’s groundbreaking work suggested a radical idea: that a microbe, Helicobacter pylori, played a major role in many peptic ulcers.1 There were significant headwinds to the proposal that microbes may be the underlying cause. In fact, Marshall and Warren’s original H. pylori research abstract in 1983 was not accepted for presentation. A few years later, they received the Nobel Prize. This story highlights the power of microbes and the concept that the microbiome may have an impact on diseases that do not seem intuitive, both in the GI tract and beyond.
Although the majority of data and clinical experience for FMT are for the prevention of recurrent Clostridioides difficile infection (rCDI), there has been a rapid growth in translational research examining the role of the microbiome in many diseases and preliminary investigation of fecal microbiota transplantation (FMT) in a number of microbiome-mediated clinical conditions. The following sections serve as a current state-of-the-field to outline the most promising indication for FMT and microbiome therapies. In the pages ahead, we outline the evidence for other CDI phenotypes, such as primary CDI and severe and fulminant disease, and also navigate the data for inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). Additionally, we move beyond the GI tract and explore the gut–liver axis, gut–brain axis, decolonization of antibiotic-resistant bacteria, and even the role of FMT for metabolic conditions, such as obesity. This overview represents the tip of the proverbial iceberg as scientists and physicians continue to explore this nascent field.
FMT for these conditions is still investigational. Data will continue to emerge and potentially transform our approach to patients suffering from microbiome-mediated diseases.
1. Pincock S. Nobel Prize winners Robin Warren and Barry Marshall. Lancet. 2005;366(945). doi:10.1016/S0140-6736(05)67587-3