Literature DB >> 21970527

Probiotic upregulation of peripheral IL-17 responses does not exacerbate neurological symptoms in experimental autoimmune encephalomyelitis mouse models.

Toshihide Kobayashi1, Tomomi Suzuki, Rumi Kaji, Masaki Serata, Tsuyoshi Nagata, Minoru Ando, Ryoko Iizuka, Satoshi Tsujibe, Junta Murakami, Junko Kiyoshima-Shibata, Ikuo Kato, Masanobu Nanno, Kan Shida.   

Abstract

CONTEXT: 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.
CONCLUSION: 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.

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Year:  2011        PMID: 21970527     DOI: 10.3109/08923973.2010.617755

Source DB:  PubMed          Journal:  Immunopharmacol Immunotoxicol        ISSN: 0892-3973            Impact factor:   2.730


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