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The gastrointestinal microbiota in the development of ME/CFS: a critical view and potential perspectives
Andreas Stallmach1, Stefanie Quickert1, Christian Puta2,3,4
1Department of Internal Medicine IV (Gastroenterology, Hepatology, and Infectious Diseases), Jena University Hospital, Jena, Germany.
Abstract:
Like other infections, a SARS-CoV-2 infection can also trigger Post-Acute Infection Syndromes (PAIS), which often progress into myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). ME/CFS, characterized by post-exercise malaise (PEM), is a severe multisystemic disease for which specific diagnostic markers or therapeutic concepts have not been established. Despite numerous indications of post-infectious neurological, immunological, endocrinal, and metabolic deviations, the exact causes and pathophysiology remain unclear. To date, there is a paucity of data, that changes in the composition and function of the gastrointestinal microbiota have emerged as a potential influencing variable associated with immunological and inflammatory pathways, shifts in ME/CFS. It is postulated that this dysbiosis may lead to intestinal barrier dysfunction, translocation of microbial components with increased oxidative stress, and the development or progression of ME/CFS. In this review, we detailed discuss the findings regarding alterations in the gastrointestinal microbiota and its microbial mediators in ME/CFS. When viewed critically, there is currently no evidence indicating causality between changes in the microbiota and the development of ME/CFS. Most studies describe associations within poorly defined patient populations, often combining various clinical presentations, such as irritable bowel syndrome and fatigue associated with ME/CFS. Nevertheless, drawing on analogies with other gastrointestinal diseases, there is potential to develop strategies aimed at modulating the gut microbiota and/or its metabolites as potential treatments for ME/CFS and other PAIS. These strategies should be further investigated in clinical trials.
Insights
SARS-CoV-2 infections can lead to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). While gut microbiota changes are associated with ME/CFS, causality is not yet proven, but offers potential therapeutic avenues.
Area of Science:
- Microbiology
- Immunology
- Neurology
Background:
- Post-Acute Infection Syndromes (PAIS) can develop after SARS-CoV-2 infection, sometimes progressing to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS).
- ME/CFS is a severe multisystemic disease characterized by post-exercise malaise (PEM), with unclear pathophysiology despite suspected neurological, immunological, and metabolic changes.
- The role of the gastrointestinal microbiota in ME/CFS is under investigation, with potential links to immune and inflammatory pathways.
Purpose of the Study:
- To review current findings on alterations in the gastrointestinal microbiota and its mediators in ME/CFS.
- To critically evaluate the evidence for a causal link between gut dysbiosis and ME/CFS development.
- To explore the potential of microbiota-targeted therapies for ME/CFS and other PAIS.
Main Methods:
- Literature review of studies examining gastrointestinal microbiota composition and function in ME/CFS patients.
- Critical analysis of existing data, considering patient population heterogeneity and study limitations.
- Drawing analogies from other gastrointestinal diseases to inform potential therapeutic strategies.
Main Results:
- Alterations in gut microbiota composition and function are frequently reported in ME/CFS.
- Current evidence primarily shows associations, not causality, between gut dysbiosis and ME/CFS.
- Studies often involve poorly defined patient groups, complicating interpretation.
Conclusions:
- While gut dysbiosis is associated with ME/CFS, a causal relationship is not established.
- Modulating the gut microbiota and/or its metabolites presents a potential therapeutic strategy for ME/CFS and PAIS.
- Further clinical trials are necessary to investigate the efficacy of these microbiota-targeted interventions.
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