, Volume 15, Issue 1, pp 68–74 | Cite as

Intestinal Permeability in Relapsing-Remitting Multiple Sclerosis

  • M. C. Buscarinu
  • S. Romano
  • R. Mechelli
  • R. Pizzolato Umeton
  • M. Ferraldeschi
  • A. Fornasiero
  • R. Reniè
  • B. Cerasoli
  • E. Morena
  • C. Romano
  • N. D. Loizzo
  • R. Umeton
  • M. Salvetti
  • G. Ristori


Changes of intestinal permeability (IP) have been extensively investigated in inflammatory bowel diseases (IBD) and celiac disease (CD), underpinned by a known unbalance between microbiota, IP and immune responses in the gut. Recently the influence of IP on brain function has greatly been appreciated. Previous works showed an increased IP that preceded experimental autoimmune encephalomyelitis development and worsened during disease with disruption of TJ. Moreover, studying co-morbidity between Crohn's disease and MS, a report described increased IP in a minority of cases with MS. In a recent work we found that an alteration of IP is a relatively frequent event in relapsing-remitting MS, with a possible genetic influence on the determinants of IP changes (as inferable from data on twins); IP changes included a deficit of the active mechanism of absorption from intestinal lumen. The results led us to hypothesize that gut may contribute to the development of MS, as suggested by another previous work of our group: a population of CD8+CD161high T cells, belonging to the mucosal-associated invariant T (MAIT) cells, a gut- and liver-homing subset, proved to be of relevance for MS pathogenesis. We eventually suggest future lines of research on IP in MS: studies on IP changes in patients under first-line oral drugs may result useful to improve their therapeutic index; correlating IP and microbiota changes, or IP and blood-brain barrier changes may help clarify disease pathogenesis; exploiting the IP data to disclose co-morbidities in MS, especially with CD and IBD, may be important for patient care.


Multiple sclerosis Intestinal permeability Mucosal-associated invariant T (MAIT) cells Autoimmune comorbidity Celiac disease Crohn’ disease 

Supplementary material

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Copyright information

© The American Society for Experimental NeuroTherapeutics, Inc. 2017

Authors and Affiliations

  • M. C. Buscarinu
    • 1
  • S. Romano
    • 1
  • R. Mechelli
    • 1
  • R. Pizzolato Umeton
    • 2
  • M. Ferraldeschi
    • 3
  • A. Fornasiero
    • 1
  • R. Reniè
    • 1
  • B. Cerasoli
    • 1
  • E. Morena
    • 1
  • C. Romano
    • 1
  • N. D. Loizzo
    • 1
  • R. Umeton
    • 4
  • M. Salvetti
    • 1
    • 5
  • G. Ristori
    • 1
  1. 1.Centre for Experimental Neurological Therapies, Department of Neurosciences, Mental Health and Sensory Organs, Faculty of Medicine and PsychologySapienza UniversityRomeItaly
  2. 2.Department of NeurologyUniversity of Massachusetts Medical SchoolWorcesterUSA
  3. 3.Department of Neurology and PsychiatrySapienza UniversityRomeItaly
  4. 4.Department of InformaticsDana-Farber Cancer InstituteBostonUSA
  5. 5.IRCCS Istituto Neurologico Mediterraneo (INM) NeuromedPozzilliItaly

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