| Gungor B, et al. (2016) (108) |
30 patients vs. 10 controls |
16S rRNA (V4) sequencing |
Marvinbryantia was significantly lower in the upper motor neuron (UMN) bowel dysfunction group than in the lower motor neuron (LMN) group after spinal cord injury(SCI). Compared with healthy groups, Roseburia, Pseudobutyrivibrio, and Megamonas were significantly lower in the LMN bowel dysfunction group; the abundances of Pseudobutyrivibrio, Dialister, and Megamonas genera were significantly lower in the UMN bowel dysfunction group.
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| Zhang C, et al. (2018) (109) |
43 patients vs. 23 controls |
16S rRNA (V3-V4) sequencing |
SCI contributed to the increased abundance of Veillonellaceae and Prevotellaceae and the decreased abundance of Bacteroidaceae and Bacteroides. The abundance of Bacteroidaceae and Bacteroides in the quadriplegia group and Acidaminococcaceae, Blautia, Porphyromonadaceae, and Lachnoclostridium in the paraplegia group were significantly higher compared to the healthy male group. Following SCI, the gut microbiota composition was significantly associated with serum biomarkers (glucose, high-density lipoprotein, creatinine, and C-reactive protein), neurogenic bowel dysfunction defecation time, and course.
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| Lin R, et al. (2020) (110) |
23 patients vs. 23 controls |
16S rRNA (V3-V4) sequencing |
There were no significant differences in the α-diversity indices of the fecal microbiota between the SCI and control groups. The abundances of Parabacteroides, Alistipes, Phascolarctobacterium, Christensenella, Barnesiella, Holdemania, Eggerthella, Intestinimonas, Gordonibacter, Bilophila, Flavonifractor, and Coprobacillus were higher in the patients with SCI than those in the healthy control.
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| Li J, et al. (2020) (111) |
32 patients (7 acute SCI and 25 long-standing SCI) vs. 25controls |
16S rRNA (V4) sequencing |
Compared with the controls, SCI patients had higher abundances of the Erysipelotrichaceae, Acidaminococcaceae, Rikenellaceae, Lachnospiraceae, Rikenellaceae, the Ruminococcaceae families. The long-standing SCI patients had higher abundances of Lachnospiraceae and Eggerthellaceae, and lower abundances of Campylobacteraceae than the controls. The acute SCI has a higher abundance of the Desulfovibrionaceae family than the controls.
|
| Bazzocchi G, et al. (2021) (112) |
100 patients |
16S rRNA (V3-V4) sequencing |
The SCI-induced gut microbiota composition showed distinct dysbiotic signatures with an enriched in potentially pathogenic, pro-inflammatory, and mucus-degrading bacteria and a decreased abundance of short-chain fatty acids (SCFAs) producers. The gut microbiota dysbiosis is very likely secondary to injury and closely related to the lesion’s degree of completeness and severity after SCI.
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| Yu B, et al. (2021) (113) |
45 patients (21 complete thoracic SCI and 24 incomplete thoracic SCI) vs. 24 controls |
16S rRNA sequencing |
Compared with healthy individuals, Actinobacteria and Synergistetes were significantly enriched in patients with complete thoracic SCI. Similarly, Bacteroidetes, Cyanobacteria, and Proteobacteria were significantly lower in patients with incomplete thoracic SCI than healthy controls. Coriobacteriaceae, Synergistetes, Eubacterium, and Cloacibacillus, were significantly increased in patients with complete thoracic SCI, while Lactobacillaceae, Lachnospiraceae, Eubacterium, Clostridium, and Sutterella, were significantly increased in patients with incomplete thoracic SCI.
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| Kigerl KA, et al. (2016) (25) |
T9 contusion mice model |
16S rRNA (V4-V5) sequencing |
SCI increased intestinal permeability and bacterial translocation from the gut, associated with immune cell activation in gut-associated lymphoid tissues (GALTs) and the altered gut microbiota composition. In naive mice, gut dysbiosis induced by oral delivery of broad-spectrum antibiotics before SCI exacerbated neurological impairment and spinal cord pathology after SCI. SCI mice treated by commercial probiotics (VSL#3) enriched lactic acid-producing bacteria, triggering a protective immune response in GALTs and conferring neuroprotection with improved neurological recovery.
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| O’Connor G, et al. (2018) (114) |
T9 contusion rat model |
16S rRNA (V4) sequencing |
Lactobacillus intestinalis, Clostridium disporicum, and Bifidobacterium choerinum were enriched, while Clostridium saccharogumia was depleted following SCI. Levels of interleukin-1β(IL-1β), IL-12, and macrophage inflammatory protein-2 significantly correlated with changes in β diversity 8-weeks post-SCI.
|
| Myers SA, et al. (2019) (115) |
T9 contusion mice model |
16S rRNA (V4) sequencing |
SCI led to an increased abundance of Proteobacteria. The absence of Pde4b improved white matter sparing and recovery of hindlimb locomotion following SCI. Moreover, SCI-induced gut dysbiosis, bacterial overgrowth, and endotoxemia were also reduced in Pde4b-/- mice.
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| Jing Y, et al. (2019) (116) |
T10 contusion mice model |
16S rRNA (V3-V4) sequencing |
Daily intraperitoneal injection with melatonin improved enhanced barrier integrity and gastrointestinal motility, reduced proinflammatory cytokines, and promoted locomotor recovery. Melatonin-treated SCI animals decreased the abundance of Clostridiales and increased the quantity of Lactobacillales and Lactobacillus. Before surgery, gut dysbiosis induced by broad-spectrum antibiotics exacerbated neurological impairment following SCI, and melatonin treatment improved locomotor recovery and intestinal integrity in antibiotic-treated SCI mice.
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| Schmidt EKA, et al. (2020) (117) |
C5 contusion rat model |
16S rRNA (V4) sequencing |
|
| Jing Y, et al. (2021) (118) |
T10 contusion mice model |
16S rRNA (V4) sequencing & HPLC-MS |
FMT-treated SCI mice facilitated functional recovery, promoted neuronal axonal regeneration, and enhanced intestinal barrier integrity and gastrointestinal motility, which short-chain fatty acids (SCFAs) and Nuclear Factor-κB (NF-κB) signaling may mediate. Butyricimonas were reduced in SCI mice, and FMT significantly reshaped gut microbiota.
|
| Schmidt EKA, et al. (2021) (119) |
C5 contusion rat model |
16S rRNA (V4) sequencing |
Minocycline had a profound acute effect on the gut microbiota diversity and composition after SCI. Gut dysbiosis following SCI has been linked to the development of anxiety-like behavior, which was also alleviated by minocycline. Although minocycline attenuated SCI-induced microglial activation, it did not change the lesion size or promote neurological recovery.
|
| Doelman A, et al. (2021) (120) |
T2 or T10 contusion pig model |
16S rRNA (V3-V4) sequencing |
In the acute phase (<14d post-SCI), Proteobacteria, Tenericutes, Epsilonbacteraeota, and Cyanobacteria decreased compared to the controls while Bacteroidetes, Firmicutes, and Spirochaetes were enriched. In the sub-acute phase (>14 days post-SCI), the abundance of Spirochaetes, Cyanobacteria, and Proteobacteria remained statistically significantly different from the controls.
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| Rong Z, et al. (2021) (121) |
T10 contusion mice model |
– |
The levels of pro-inflammatory cytokines tumor necrosis factor-α, IL-1β, and IL-6 in SCI mice were increased, while the levels of anti-inflammatory factors IL-4, transforming growth factor-β, and IL-10 were decreased. Gut microbiota dysbiosis aggravated SCI by activating the toll-like receptor 4(TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway.
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| Du J, et al. (2021) (122) |
T4 or T10 contusion mice model |
genome- and gene-resolved metagenomic analysis |
The abundance of Lactobacillus johnsonii and CAG-1031 spp. decreased, while Weissella cibaria, Lactococcus lactis_A, Bacteroides thetaiotaomicron were enriched after SCI. Microbial-mediated biosynthesis of tryptophan, vitamin B6, and folate was reduced after SCI. 1028 mostly novel viral populations were recovered, which expanded known murine gut viral species sequence space. Phages of beneficial commensal hosts, including CAG-1031, Lactobacillus, and Turicibacter, decreased, while phages of pathogenic hosts, including Weissella, Lactococcus, and class Clostridia, increased after SCI.
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