The role of faecal microbiota transplantation: looking beyond Clostridioides difficile infection

Abstract

Faecal microbiota transplantation (FMT) is the transfer of screened and minimally processed faecal material from a ‘healthy’ donor to ‘diseased’ recipient. It has an established role, and is recommended as a therapeutic strategy, in the management of recurrent Clostridioides difficile infection (CDI). Recognition that gut dysbiosis is associated with, and may contribute to, numerous disease states has led to interest in exploiting FMT to ‘correct’ this microbial imbalance. Conditions for which it is proposed to be beneficial include inflammatory bowel disease, irritable bowel syndrome, liver disease and hepatic encephalopathy, neuropsychiatric conditions such as depression and anxiety, systemic inflammatory states like sepsis, and even coronavirus disease 2019. To understand what role, if any, FMT may play in the management of these conditions, it is important to consider the potential risks and benefits of the therapy. Regardless, there are several barriers to its more widespread adoption, which include incompletely understood mechanism of action (especially outside of CDI), inability to standardise treatment, disagreement on its active ingredients and how it should be regulated, and lack of long-term outcome and safety data. Whilst the transfer of faecal material from one individual to another to treat ailments or improve health has a history dating back thousands of years, there are fewer than 10 randomised controlled trials supporting its use. Moving forward, it will be imperative to gather as much data from FMT donors and recipients over as long a timeframe as possible, and for trials to be conducted with rigorous methodology, including appropriate control groups, in order to best understand the utility of FMT for indications beyond CDI. This review discusses the history of FMT, its appreciable mechanisms of action with reference to CDI, indications for FMT with an emerging evidence base above and beyond CDI, and future perspectives on the field.

Global Research Trends in Irritable Bowel Syndrome: A Bibliometric and Visualized Study

“…FMT involves the application of a fecal solution from a healthy contributor into the gut of a receiver that is aimed at restoring a dysfunctional microbial composition to a healthy one, and so to improve the function of the gut microbiota. In addition to its commonly recommended use in Clostridioides difficile infection, FMT has also recently gained attention due to the strong evidence linking dysbiosis to IBS pathogenesis ( 117 ). No consensus exists regarding FMT procedure, different routes of FMT delivery (e.g., colonoscopy, nasogastric tube, enema, and oral capsules), the types of formulations (frozen, dried and fresh), and the number and type of donors were examined.…”

Effect of fecal microbiota transplantation on the TGF-β1/Smad signaling pathway in rats with TNBS-induced colitis

“…FMT has been proven to be highly successful in the treatment of recurrent and antibiotic refractory Clostridioides difficile infections, with a cure rate of up to 90% (22)(23)(24). Thus, FMT has become a promising therapeutic approach to correct IBD-related dysbiosis (25,26). FMT has been proven to be efficacious in treating IBD; however, its mechanism of action remains unclear.…”

Recurrent Campylobacter jejuni Infection in an Immunodeficient Patient Treated with Repeated Faecal Microbiota Transplant (FMT)—A Case Report

“…There are also higher levels of plasma lipopolysaccharide and markers of immune activation (e.g., soluble CD14 and CD25), suggesting the breakdown of the gut barrier and disordered microbiota-mucosal immunity [ 20 ]. FMT is proposed to work (at least in the context of C. difficile ) to increase bacterial diversity with an ensuing increase in short-chain fatty acid production and secondary bile acid production, restore gut barrier integrity, and modulate microbiota–mucosal immune interplay, including the production of antimicrobial peptides [ 21 ]. These alterations promote colonisation resistance to enteropathogens.…”