Page 23 - AN-2-3

Advanced Neurology The role of gut in multiple sclerosis

including Bacteroides, Odoribacter, Lactobacillus, 4.2. Antibiotics
Sutterella, and Bifidobacterium [77-79] . Probiotic use also In mice models, antibiotic intervention in the gut
reduced the abundance of strains previously linked to MS microbiota is currently yielding positive results.
intestinal dysbiosis such as Akkermansia and Blautia [80] . Researchers report that oral prophylactic antibiotics
Two commercial multi-species probiotics, Lactibianeiki during the presymptomatic transition phase, in particular,
and Vivomixx, induce peripheral immune tolerance in prevented motor dysfunction in TMEV mice and reduced
EAE mice by regulating DC number and phenotype. susceptibility to EAE; however, antibiotic treatment
The Lactibianeiki group had a higher frequency of Tregs after an EAE episode did not reduce the severity of the
with a lower frequency of plasma cells [78] . Furthermore, illness [88,89] . Clostridium butyricum and norfloxacin,
oral Vivomixx inhibited the proliferation of microglia, as gut microbiota interventions, may alleviate EAE by
astrocytes, and leukocyte infiltration, while activating inhibiting the Th17/Treg-related pathway. Treatment with
the proliferation of regulatory B cells (Bregs) in Clostridium butyricum reduced the number of Th1 cells in
the CNS of TMEV mice [77] . It is worth noting that the spleen . According to a recent study, oral ampicillin
[90]
Lactibianeiki and Vivomixx are commercial products therapy reduced the severity of EAE. Researchers also
that can be quickly translated into clinical use. In mice, discovered two molecules produced by Lactobacillus reuteri
a kind of probiotic, Lactobacillus acidipiscis, induced the and a newly discovered strain of the Erysipelotrichaceae
generation of γδ1 Treg cells and CD4 Foxp3 Treg cells family that work together to cause the accumulation of
+
+
+
while inhibiting the differentiation of cerebrospinal Th1 MOG-specific Th17 cells in the small bowel . The data
[86]
as well as Th17 cells [81] . Oral probiotics also can modulate also support a link of the gut-microbiota-CNS axis.
immune cells, inhibit pro-inflammatory cytokine
expression such as IL-1/6/17, and IFN-γ, and promote There is not much research on the impact of antibiotic
the anti-inflammatory cytokine IL-10 expression in EAE therapy on MS. In comparison to IFN-β-only therapy,
mice [77,82,83] . two small studies looking at the effects of doxycycline and
IFN-β in MS found lower rates of relapse, better indices
Probiotic treatment has only been tested in three of disability, and fewer gadolinium-enhancing lesions [91,92] .
research addressing MS, and there are few human studies Minocycline delayed the conversion of patients with
on the subject. In two small double-blinded randomized clinically isolated syndrome (CIS) to MS during a
controlled trials (RCTs), the MS group receiving a 6-month but not a 24-month timeframe, according to
combination of Lactobacillus and Bifidobacterium every day another double-blind, randomized trial . A bigger
[93]
for 12 weeks displayed meaningful ameliorations among investigation into those with CIS is continuing (Clinical
disability score, depression, anxiety, and inflammatory Trial NCT04291456). Indeed, one study found that using
markers, with decreased IL-8 and TNF-α expression of ampicillin during clinical EAE worsened the disease,
peripheral blood mononuclear cells [84,85] . Similarly, Tankou whereas using vancomycin had no clinical effect . There
[61]
et al. discovered a reduction of CD80 protein production are dangers associated with continuous antibiotic treatment
in peripheral monocytes after giving MS patients as well for MS, including the growth of fungus, opportunistic
as HCs a probiotic combination including Lactobacillus, pathogens such as Clostridium difficile, and antibiotic-
Bifidobacterium, and Streptococcus twice daily for 2 months. resistant infections .
[94]
After taking probiotics, the documented modifications to
the immune system and gut microbiota composition were 4.3. Diet
not sustained . Diet has a significant impact on the gastrointestinal tract,
[80]
An analysis of GF mice mono-colonized with a and dietary treatments can help to correct intestinal
new strain of the Erysipelotrichaceae family, however, microflora imbalances [95-97] . A study in marmosets
revealed that Lactobacillus reuteri treatment increased showed that a targeted dietary intervention lowers pro-
MOG-specific responses. It was suggested that the inflammatory T cells that respond to recombinant human
molecular similarity between MOG and the uvrA gene MOG and improves brain remyelination . Another study,
[98]
product of Lactobacillus reuteri could be the mechanism by taking mice on intermittent fasting (IF), found that IF
causing EAE exacerbation . Following the study, it is improved the clinical course and pathology of EAE in mice
[86]
important to take into account the synergistic impact by improving intestinal dysregulation, which increased
that these microorganisms have when determining the microbial abundance and enrichment, increasing ketone
pathogenicity of MS. Similarly, another study discovered formation and glutathione metabolism, and enhancing
that Lactobacillus reuteri aggravated EAE in mice with antioxidant pathways, leading to less inflammation,
certain genetic predispositions . demyelination, and axonal damage .
[87]
[99]
Volume 2 Issue 3 (2023) 6 https://doi.org/10.36922/an.413