Cited by 96Gut microbiota and healthMultiple Sclerosis Research StudiesProbiotics and Fermented Foods

Gut Microbiota Interventions With Clostridium butyricum and Norfloxacin Modulate Immune Response in Experimental Autoimmune Encephalomyelitis Mice

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Chen, Hao, Ma, Xiaomeng, Liu, Yingying, Ma, Lili, Chen, Zhaoyu, Lin, Xiuli, Si, Lei, Ma, Xueying +1 more·2019·Frontiers in Immunology

Abstract

Gut microbiota has been proposed as an important environmental factor which can intervene and modulate CNS autoimmunity. Here, we altered the composition of gut flora with C. butyricum and norfloxacin in experimental autoimmune encephalomyelitis (EAE), an animal model of Multiple sclerosis. We found that appropriate C. butyricum (5.0×106 CFU/mL intragastrically/daily, staring at weaning period of age) and norfloxacin (5 mg/kg intragastrically/daily, one week prior to EAE induction) treatment could both ameliorate EAE although there are obvious differences in gut microbiota composition between these two interventions. C. butyricum increased while norfloxacin decreased the abundance and diversity of the gut microbiota in EAE mice, and both of the treatments decreased firmicutes/bacteroidetes ratio. In the genus level, C. butyricum treatment increased the abundance of Prevotella while Akkermansia and Allobaculum increased in norfloxacin treatment. Moreover, both interventions reduced Desulfovibroneceae and Ruminococcus species. Although the discrepancy in the gut microbiota composition with the two interventions, C. butyricum and norfloxacin treatment both reduced Th17 response and increased Treg response in the gastrointestinal tract and extra-gastrointestinal organ systems in EAE mice. And the reduced activity of p38 MARK and JNK signaling in spinal cord could be observed in the two interventions. The results suggested that manipulation of gut microbiota interventions should consider many factors such as timing, duration and dosage. The discrepancy in the composition and the similar protective T cells response of C. butyricum and norfloxacin imply that achieving intestinal microecology balance by promoting and/or stimulating the gut microbiota contribute to the well-being of immune response in EAE mice.

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Authors
Chen, H., Ma, X., Liu, Y., Ma, L., Chen, Z., Lin, X., Si, L., Ma, X., & Chen, X.
Affiliations
Third Affiliated Hospital of Sun Yat-sen University (CN)
Corresponding author
Chen, Xiaohong
Venue
Frontiers in Immunology
Published
2019-07-23
Volume
10
Pages
1662-1662
ISSN
1664-3224 (ISSN-L)
OpenAlex
W2955396625
Cited by
96
References
63
Citations by year
2026: 8 · 2025: 10 · 2024: 23 · 2023: 16 · 2022: 11 · 2021: 13 · 2020: 13 · 2019: 1
FWCI
3.14
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Immunology (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China (813111290)
  • Israel Science Foundation (813111290)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Probiotics and Fermented Foods
Keywords
gut microbiota, Clostridium butyricum, norfloxacin, experimental autoimmune encephalomyelitis, multiple sclerosis, central nervous system autoimmunity, Th17/Treg balance, p38 MAPK signaling, JNK signaling, Prevotella, Akkermansia, Firmicutes/Bacteroidetes ratio, gut-brain axis
MeSH terms
Bacillota, Gastrointestinal Microbiome, Animals, Bacteroidaceae, Encephalomyelitis, Autoimmune, Experimental, Female, Mice, Inbred C57BL, Nerve Tissue Proteins, Norfloxacin, Random Allocation, Specific Pathogen-Free Organisms, Spinal Cord, Signal Transduction, Lymphocyte Count, Probiotics, Clostridium butyricum, JNK Mitogen-Activated Protein Kinases, p38 Mitogen-Activated Protein Kinases, T-Lymphocytes, Regulatory, Mice, Th17 Cells

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