Microbiome in Multiple Sclerosis: Where Are We, What We Know and Do Not Know

Boziki, Marina; Kesidou, Evangelia; Theotokis, Paschalis; Mentis, Alexios‐Fotios A.; Karafoulidou, Eleni; Melnikov, Mikhail; Sviridova, Anastasiya; Rogovski, Vladimir; Boyko, A. N.; Grigoriadis, Nikolaos

doi:10.3390/brainsci10040234

Cited by 71 publications

(60 citation statements)

References 110 publications

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“…Additional therapy in combination with DMTs can be helpful. The modification of gut microbiota may serve as an additional therapeutic strategy in promoting treatment effectiveness and optimal response [ 36 ].…”

Section: Discussionmentioning

confidence: 99%

Assessment of Disability Progression Independent of Relapse and Brain MRI Activity in Patients with Multiple Sclerosis in Poland

Kapica-Topczewska

Collin²,

Tarasiuk

et al. 2021

JCM

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The aim of the study was to verify the association of clinical relapses and brain activity with disability progression in relapsing/remitting multiple sclerosis patients receiving disease-modifying treatments in Poland. Disability progression was defined as relapse-associated worsening (RAW), progression independent of relapse activity (PIRA), and progression independent of relapses and brain MRI Activity (PIRMA). Data from the Therapeutic Program Monitoring System were analyzed. Three panels of patients were identified: R0, no relapse during treatment, and R1 and R2 with the occurrence of relapse during the first and the second year of treatment, respectively. In the R0 panel, we detected 4.6% PIRA patients at 24 months (p < 0.001, 5.0% at 36 months, 5.6% at 48 months, 6.1% at 60 months). When restricting this panel to patients without brain MRI activity, we detected 3.0% PIRMA patients at 12 months, 4.5% at 24 months, and varying from 5.3% to 6.2% between 36 and 60 months of treatment, respectively. In the R1 panel, RAW was detected in 15.6% patients at 12 months and, in the absence of further relapses, 9.7% at 24 months and 6.8% at 36 months of treatment. The R2 group was associated with RAW significantly more frequently at 24 months compared to the R1 at 12 months (20.7%; p < 0.05), but without a statistical difference later on. In our work, we confirmed that disability progression was independent of relapses and brain MRI activity.

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Section: Discussionmentioning

confidence: 99%

Assessment of Disability Progression Independent of Relapse and Brain MRI Activity in Patients with Multiple Sclerosis in Poland

Kapica-Topczewska

Collin²,

Tarasiuk

et al. 2021

JCM

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“…Particularly, EVs derived from stem/progenitor cells have been reported to inhibit proliferation and activation of immune cell and promote immune tolerance [ 25 , 26 ]. In this context, a role of placental EVs in the stem cells-microbiome connection could also be hypothesized [ 27 , 28 ]. On the other hand, almost all EV samples were negative for several surface proteins expressed by antigen-presenting cells (HLA-A/B/C molecules, CD86, and CD1c), mature or activated T cells (CD2, CD3, CD25), activated immune cells with cytotoxic properties (CD56), and B cells (CD19, CD20).…”

Section: Discussionmentioning

confidence: 99%

A First Phenotypic and Functional Characterization of Placental Extracellular Vesicles from Women with Multiple Sclerosis

Martire

Montarolo

Spadaro

et al. 2021

IJMS

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Pregnancy is a unique situation of physiological immunomodulation, as well as a strong Multiple Sclerosis (MS) disease modulator whose mechanisms are still unclear. Both maternal (decidua) and fetal (trophoblast) placental cells secrete extracellular vesicles (EVs), which are known to mediate cellular communication and modulate the maternal immune response. Their contribution to the MS disease course during pregnancy, however, is unexplored. Here, we provide a first phenotypic and functional characterization of EVs isolated from cultures of term placenta samples of women with MS, differentiating between decidua and trophoblast. In particular, we analyzed the expression profile of 37 surface proteins and tested the functional role of placental EVs on mono-cultures of CD14+ monocytes and co-cultures of CD4+ T and regulatory T (Treg) cells. Results indicated that placental EVs are enriched for surface markers typical of stem/progenitor cells, and that conditioning with EVs from samples of women with MS is associated to a moderate decrease in the expression of proinflammatory cytokines by activated monocytes and in the proliferation rate of activated T cells co-cultured with Tregs. Overall, our findings suggest an immunomodulatory potential of placental EVs from women with MS and set the stage for a promising research field aiming at elucidating their role in MS remission.

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“…As previously emphasized, ILC3 have a central role in controlling the interaction between the gut microbiota and the host immune system. MS patients were shown to have altered gut microbiota composition, and the alterations were associated with MS pathogenesis [reviewed in (84)]. Some studies directly showed the influence of MS gut microbiota on CNS autoimmunity.…”

Section: Untangling Potency Of Gut Ilc3 Modulation For Ms Therapymentioning

confidence: 99%

ILC3, a Central Innate Immune Component of the Gut-Brain Axis in Multiple Sclerosis

et al. 2021

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Gut immune cells have been increasingly appreciated as important players in the central nervous system (CNS) autoimmunity in animal models of multiple sclerosis (MS). Among the gut immune cells, innate lymphoid cell type 3 (ILC3) is of special interest in MS research, as they represent the innate cell counterpart of the major pathogenic cell population in MS, i.e. T helper (Th)17 cells. Importantly, these cells have been shown to stimulate regulatory T cells (Treg) and to counteract pathogenic Th17 cells in animal models of autoimmune diseases. Besides, they are also well known for their ability to stabilize the intestinal barrier and to shape the immune response to the gut microbiota. Thus, proper maintenance of the intestinal barrier and the establishment of the regulatory milieu in the gut performed by ILC3 may prevent activation of CNS antigen-specific Th17 cells by the molecular mimicry. Recent findings on the role of ILC3 in the gut-CNS axis and their relevance for MS pathogenesis will be discussed in this paper. Possibilities of ILC3 functional modulation for the benefit of MS patients will be addressed, as well.

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Microbiome in Multiple Sclerosis: Where Are We, What We Know and Do Not Know

Cited by 71 publications

References 110 publications

Assessment of Disability Progression Independent of Relapse and Brain MRI Activity in Patients with Multiple Sclerosis in Poland

Assessment of Disability Progression Independent of Relapse and Brain MRI Activity in Patients with Multiple Sclerosis in Poland

A First Phenotypic and Functional Characterization of Placental Extracellular Vesicles from Women with Multiple Sclerosis

ILC3, a Central Innate Immune Component of the Gut-Brain Axis in Multiple Sclerosis

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