title: Probiotic upregulation of peripheral IL-17 responses does not exacerbate neurological symptoms in experimental autoimmune encephalomyelitis mouse models.
abstract: BACKGROUND
  It is of great importance to evaluate the safety of probiotics in dysregulated immune conditions, as probiotics can possibly modulate immune functions in the host.
  
  
  OBJECTIVE
  We tried to confirm the safety of using Lactobacillus casei strain Shirota (LcS) to help prevent autoimmunity in the central nervous system.
  
  
  METHODS
  We used two chronic experimental autoimmune encephalomyelitis (EAE) models, a relapse and remission type EAE model in SJL/J mice and a durable type model in C57BL/6 mice. LcS was administered from 1 week before antigen sensitization until the end of the experiments, and neurological symptoms and histopathological changes of the spinal cord were observed. Immunological parameters were also examined in the SJL/J mouse model.
  
  
  RESULTS
  LcS administration did not exacerbate neurological symptoms or histopathological changes of the spinal cord in either model but instead tended to improve neurological symptoms in the SJL/J mouse EAE model. LcS administration transiently upregulated IL-17 production by antigen-stimulated lymphocytes of draining lymph nodes 7 days after sensitization. Enhanced production of IL-10 and an increase in the percentage of CD4(+)CD25(+) T regulatory cells were also observed at the same sites. Strong expression of IL-17 mRNA was detected in the spinal cord of mice that displayed severe neurological symptoms on day 12, but this expression was not enhanced by LcS administration.
  
  
  CONCLUSIONS
  These results demonstrate that LcS does not exacerbate, but instead may improve EAE depending on the immunization conditions, and that IL-17 responses at peripheral sites may not always result in a worsening of autoimmune diseases.
authors.affiliation: Yakult Central Institute for Microbiological Research, Tokyo, Japan.
authors.forename: Toshihide
authors.initials: T
authors.lastname: Kobayashi
authors.forename: Tomomi
authors.initials: T
authors.lastname: Suzuki
authors.forename: Rumi
authors.initials: R
authors.lastname: Kaji
authors.forename: Masaki
authors.initials: M
authors.lastname: Serata
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Nagata
authors.forename: Minoru
authors.initials: M
authors.lastname: Ando
authors.forename: Ryoko
authors.initials: R
authors.lastname: Iizuka
authors.forename: Satoshi
authors.initials: S
authors.lastname: Tsujibe
authors.forename: Junta
authors.initials: J
authors.lastname: Murakami
authors.forename: Junko
authors.initials: J
authors.lastname: Kiyoshima-Shibata
authors.forename: Ikuo
authors.initials: I
authors.lastname: Kato
authors.forename: Masanobu
authors.initials: M
authors.lastname: Nanno
authors.forename: Kan
authors.initials: K
authors.lastname: Shida
mesh_terms: D000818:Animals; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000473:pathology; D005260:Female; D016753:Interleukin-10 / Q000276:immunology; D020381:Interleukin-17 / Q000276:immunology*; D007780:Lacticaseibacillus casei; D051379:Mice; D019936:Probiotics / Q000494:pharmacology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000473:pathology; D015854:Up-Regulation / Q000276:immunology*
chemical_list: C556062:IL10 protein, mouse; D020381:Interleukin-17; D016753:Interleukin-10