Abstract
The gut microbiota regulates the host immune and nervous systems and plays an important role in the pathogenesis of autoimmune neurological disease multiple sclerosis (MS). There are considerable efforts currently being undertaken to develop therapies for MS based on the modulation of microbiota. Evidence from experimental models suggests that the manipulation of microbiota through diet or antibiotics prior to the disease development limits disease susceptibility. However, it is currently unclear if microbiota manipulation therapies would also have an impact on ongoing neurological disease. Here, we examined the effect of antibiotic-based microbiota modulation in spontaneous experimental autoimmune encephalomyelitis (EAE) mouse models of MS before and after the onset of autoimmune disease. Prophylactic antibiotic treatment led to a significant reduction of susceptibility to spontaneous EAE. In contrast, antibiotic treatment after the onset of spontaneous EAE did not show a significant amelioration. These results reveal that the perturbation of gut bacteria alters disease susceptibility but has minimal impact on the ongoing neurological disease.
Highlights
Advances in Deoxyribonucleic acid (DNA) sequencing and bioinformatics technologies in the last two decades led to an exponential increase of studies that investigated the role of the microbiome, in particular, gut microbiome, in several diseases
Previous studies have shown that manipulation of microbiota with prophylactic antibiotic treatment suppressed the severity of autoimmune encephalomyelitis in actively induced EAE models [6,7,8]
Similar to previous reports in actively induced EAE models [6,7,8], prophylactic antibiotic treatment either at 2 or 4 weeks after birth suppressed the development of spontaneous EAE to a greater extent (Fig. 1c and data not shown)
Summary
Advances in DNA sequencing and bioinformatics technologies in the last two decades led to an exponential increase of studies that investigated the role of the microbiome, in particular, gut microbiome, in several diseases. This surge in interest has garnered attention in clinical settings due to their potential applications in clinical practice [1, 2]. In animal models of MS, manipulation of microbiota prior to the development of the disease either by antibiotics [6,7,8] or diet [9,10,11] modulated disease severity and incidence. Using spontaneous EAE mouse models of MS, we studied the relative
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