Gut microbiome changes over the course of multiple sclerosis differentially influence autoimmune neuroinflammation
Posted on: 14 May 2026
Preprint posted on 24 February 2026
A time‑dependent role of the gut microbiome in Multiple Sclerosis progression
Selected by Carole Djagang, Nour HAROUN, Phalica Georges, uMontreal Neuro preLighters
Categories: genomics, immunology, microbiology, neuroscience
Background
Multiple Sclerosis (MS) is a dynamic disease Multiple sclerosis (MS) is a dynamic disease characterized by continuous changes over time. During its early stages, the disease is driven primarily by inflammatory processes that lead to focal demyelinating lesions and episodic neurological symptoms¹,². While genetic factors contribute to MS susceptibility, environmental factors are believed to play a dominant role in its initiation and progression³–⁵. Notably, the gut microbiome has emerged as a critical regulator of immune responses, raising fundamental questions about whether changes in gut bacteria actively drive neurological disease or instead reflect secondary consequences of chronic inflammation ⁶–¹¹.
Although gut microbiome alterations (dysbiosis) have been consistently reported in MS patients, it remains unclear how this relationship evolves over the decades-long course of the disease. Specifically, it is unclear whether microbiome changes are causally linked to disease progression or merely correlate with disease state. Research has shown that MS patients harbor gut microbial communities distinct from those of healthy individuals. In animal models, such differences can directly influence disease severity. However, whether such microbiota-driven immune effects persist throughout the disease or are confined to earlier stages remains an open question.
In this context, the present study focuses on a specific cohort of relapsing-remitting MS (RRMS) patients, using a 16-year disease duration threshold to distinguish between “early” and “late” stages. This stratification allows investigation of a potential temporal “window of opportunity” during which modulation of the gut microbiota may exert maximal influence on systemic immune responses and disease trajectory.
Specifically, the study asks whether the gut microbiota’s capacity to shape immune regulation evolves over the course of MS, and whether this evolution parallels the shift from peripheral inflammation to compartmentalized neurodegeneration within the central nervous system. The researchers hypothesize that during early MS (Short-MS), the gut microbiota acts as a key driver of systemic pro-inflammatory responses, whereas this influence diminishes as the disease progresses and pathology becomes increasingly CNS-compartmentalized. Implicitly, this raises the possibility that microbiome-derived signatures could serve as stage-specific biomarkers, potentially informing prognosis or therapeutic timing.
Key Findings
Mice were treated with antibiotics to eliminate their original microbiota and then received three consecutive transplants from human donors to restore it (preprint Fig. 3A). Each faecal sample used for transplantation came from one of three groups (controls, short-MS, and long-MS). After 3 weeks, faecal samples were taken to make sure that the microbiota from human donors was able to implant itself correctly to the gastrointestinal tract of the recipient.
Short-MS microbiota exacerbates disease severity
Mice transplanted with faecal samples demonstrated a similar disease course with a peak followed by a partial recovery period. It was, however, not the case for mice transplanted with short-MS faecal samples, which showed a higher disease burden not followed by a remission phase. (preprint Fig. 3B).
Loss of Treg-mediated regulation correlates with disease severity
FOXP3 is expressed by Treg. FoxP3+ Rorgt+ pTreg cells are directly related to the microbiota and inflammation. A decrease of FOXP3+ Treg cells and FOXP3+ Rorgt+ PTreg cells was observed in the colon of mice treated with short-MS microbiota (preprint Fig. 4F). The count of FOXP3+ Treg cells was negatively correlated with the maximum clinical score reached during the EAE development used to model neuroinflammation-related damages seen in multiple sclerosis (preprint Fig. 4G).
Short-MS microbiota promotes systemic inflammation
All faecal samples led to an increase in anti-inflammatory cytokine (IL-10) production by Peripheral Blood Mononuclear Cells (PBMCs). However, the control supernatant was a greater IL-10 inducer (preprint Fig. 5A). A higher secretion of pro-inflammatory cytokines (TNF-a and IL-17) was detected in cells stimulated only with the faecal extracts of short-MS patients (preprint Fig. 5B-C). These results show that the microbiota from short-MS patients has a greater capacity of evoking systemic inflammatory responses.
Why we highlight this preprint
This preprint really resonated with us, as it highlights how complex diseases like MS require multidisciplinary approaches. We found it particularly interesting that the gut microbiome evolves with disease stage shifting from a proinflammatory profile early on to a more balanced state later. By focusing on intra-disease variation, it offers a fresh perspective on how these changes shape immune responses and progression.
Our longstanding interest in MS stems from its clinical heterogeneity, unpredictability, and the shifting inflammatory dynamics that make RR form uniquely compelling to explore.
Additionally, this paper parallels our own work using adoptive transfer of activated T cells to induce Parkinsonism-like phenotype in germ-free mice. After encountering difficulties reproducing this model in a new animal facility, we hypothesized that differences in gut microbiota might explain this variability. The findings support our view, showing that immune activation alone is insufficient; microbial composition critically modulates neuroimmune outcomes.
Questions for the authors
1. Would it be possible to include additional control groups, such as mice that were only immunized (MOG), PTx only or those that received microbiota transfer alone, to better isolate and assess the specific influence of the microbiota on the host response?
2. Would it be possible to examine the immune cells composition within the brains of the recipient mice to more precisely identify which cellular subsets had traversed the blood–brain barrier, or to characterize the CNS‑infiltrating immune populations elicited in response to microbiota transfer? Such analyses could provide a deeper mechanistic understanding of how microbiota‑driven immune modulation shapes neuroinflammatory pathways and contributes to neurodegenerative processes
3. It is unclear whether patients discontinued immunomodulatory/suppressive therapy before fecal sampling. If not, how can you rule out that the observed microbiome profiles result from drug effects rather than disease‑related changes, especially if the agent is oral and can directly alter the mice’s response after transplantation?
References
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