Oral Administration of the Probiotic Strain Escherichia coli Nissle 1917 Reduces Susceptibility to Neuroinflammation and Repairs Experimental Autoimmune Encephalomyelitis-Induced Intestinal Barrier Dysfunction

Frontiers in Immunology

Eric Oswald¹  Isabelle Bernard²  Mehdi Benamar²  Abdelhadi Saoudi²  Sahar Kassem²  Michele Boury³  Thomas Secher³  Frederick Barreau³ 

[1] CHU Toulouse, Hôpital Purpan, Service de Bactériologie-Hygiène, Toulouse, France;Centre de Physiopathologie de Toulouse Purpan (CPTP), Université de Toulouse, UPS, INSERM, CNRS, Toulouse, France;IRSD, Université de Toulouse, INSERM, INRA, ENVT, UPS, Toulouse, France;

关键词: Escherichia coli Nissle 1917;    experimental autoimmune encephalomyelitis;    probiotic;    intestinal permeability;    encephalitogenic T-cell;    central nervous system;   

DOI  :  10.3389/fimmu.2017.01096

来源: DOAJ

【 摘 要 】

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) with an increasing incidence in developed countries. Recent reports suggest that modulation of the gut microbiota might be one promising therapy for MS. Here, we investigated whether the probiotic Escherichia coli strain Nissle 1917 (ECN) could modulate the outcome of experimental autoimmune encephalomyelitis (EAE), a murine model of MS. We evidenced that daily oral treatment with ECN, but not with the archetypal K12 E. coli strain MG1655, reduced the severity of EAE induced by immunization with the MOG35–55 peptide. This beneficial effect was associated with a decreased secretion of inflammatory cytokines and an increased production of the anti-inflammatory cytokine IL-10 by autoreactive CD4 T cells, both in peripheral lymph nodes and CNS. Interestingly, ECN-treated mice exhibited increased numbers of MOG-specific CD4+ T cells in the periphery contrasting with severely reduced numbers in the CNS, suggesting that ECN might affect T cell migration from the periphery to the CNS through a modulation of their activation and/or differentiation. In addition, we demonstrated that EAE is associated with a profound defect in the intestinal barrier function and that treatment with ECN, but not with MG1655, repaired intestinal permeability dysfunction. Collectively, our data reveal that EAE induces a disruption of the intestinal homeostasis and that ECN protects from disease and restores the intestinal barrier function.

【 授权许可】

Unknown