Abstract
The gastrointestinal (GI) tract is a complex and well-balanced milieu of anatomic and immunological barriers. The epithelial surface of the GI tract is colonized by trillions of microorganisms, known as the gut microbiota, which is considered an “organ” with distinctive endocrine and immunoregulatory functions. Dysregulation of the gut microbiota composition, termed dysbiosis, has been associated with epithelial damage and translocation of microbial products into the circulating blood. Dysbiosis, increased gut permeability and chronic inflammation play a major role on the clinical outcome of inflammatory bowel diseases, graft-vs.-host disease (GVHD) and HIV infection. In this review, we focus on GVHD and HIV infection, conditions sharing gut immune damage leading to dysbiosis. The degree of dysbiosis and level of epithelial gut damage predict poor clinical outcome in both conditions. Emerging interventions are therefore warranted to promote gut microbiota homeostasis and improve intestinal barrier function. Interventions such as anti-inflammatory medications, and probiotics have toxicity and/or limited transitory effects, justifying innovative approaches. Fecal microbiota transplantation (FMT) is one such approach where fecal microorganisms are transferred from healthy donors into the GI tract of the recipient to restore microbiota composition in patients with Clostridium difficile-induced colitis or inflammatory bowel diseases. Preliminary findings point toward a beneficial effect of FMT to improve GVHD and HIV-related outcomes through the engraftment of beneficial donor bacteria, notably those producing anti-inflammatory metabolites. Herein, we critically review the potential for FMT in alleviating dysbiosis and gut damage in patients with GVHD or HIV-infection. Understanding the underlying mechanism by which FMT restores gut function will pave the way toward novel scalable and targeted interventions.
Highlights
Trillions of microorganisms reside in the human gut, encompassing bacteria and fungi, archaea, viruses, and eukaryotic microbes, collectively termed microbiota
Recent evidence has shown that patients with diabetes, inflammatory bowel diseases (IBD), cancer, graft-vs.-host disease (GVHD) or HIV infection present with gut dysbiosis, gut damage, and microbial translocation [4,5,6,7]
These findings suggest that patients with GVHD and HIV infection share similar features in gut damage and related microbial translocation
Summary
Trillions of microorganisms reside in the human gut, encompassing bacteria and fungi, archaea, viruses, and eukaryotic microbes, collectively termed microbiota. In patients with GVHD and PLWH, CMV latent infection or reactivation is associated with poor clinical outcomes [52,53,54,55,56,57] These findings suggest that patients with GVHD and HIV infection share similar features in gut damage and related microbial translocation. GVHD patients or PLWH present with a lower abundance of SCFA-producing bacteria and a lower level of SCFAs, compared to non-GVHD HSCT patients or HIVnegative individuals, respectively [61,62,63,64] In both conditions, lower levels of SCFAs have been associated with gut damage and inflammation [62, 64,65,66]. The precise influence of different microbiota composition and metabolites on epithelial barrier and clinical outcomes remain poorly understood and need further studies to define their distinctive role on the development of GVHD and HIV infection.
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