Spinal cord injury-induced neurogenic bowel: A role for host-microbiome interactions in bowel pain and dysfunction

Willits, Adam B.; Kader, Leena; Eller, Olivia; Roberts, Emily; Bye, Bailey; Strope, Taylor; Freudenthal, Bret D.; Umar, Shahid; Chintapalli, Sree; Shankar, Kartik; Pei, Dong; Christianson, Julie A.; Baumbauer, Kyle M.; Young, Erin E.

doi:10.1016/j.ynpai.2024.100156

Cited by 2 publications

(2 citation statements)

References 93 publications

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“…This complex microbial community plays pivotal roles in host physiology, including the development and modulation of the ENS 21 – 23 . Emerging data highlight an association between the gut microbiome and locomotor recovery or pain after SCI 24 – 26 . However, the potential pathogenicity of the injury-associated microbiome and precise contributions to recovery are unknown.…”

Section: Introductionmentioning

confidence: 99%

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Diet-microbiome interactions promote enteric nervous system resilience following spinal cord injury

Hamilton,

Blackmer-Raynolds,

et al. 2024

Preprint

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Spinal cord injury (SCI) results in a plethora of physiological dysfunctions across all body systems, including intestinal dysmotility and atrophy of the enteric nervous system (ENS). Typically, the ENS has capacity to recover from perturbation, so it is unclear why intestinal pathophysiologies persist after traumatic spinal injury. With emerging evidence demonstrating SCI-induced alterations to the gut microbiome composition, we hypothesized that modulation of the gut microbiome could contribute to enteric nervous system recovery after injury. Here, we show that intervention with the dietary fiber, inulin prevents ENS atrophy and limits SCI-induced intestinal dysmotility in mice. However, SCI-associated microbiomes and exposure to specific SCI-sensitive gut microbes are not sufficient to modulate injury-induced intestinal dysmotility. Intervention with microbially-derived short-chain fatty acid (SCFA) metabolites prevents ENS dysfunctions and phenocopies inulin treatment in injured mice, implicating these microbiome metabolites in protection of the ENS. Notably, inulin-mediated resilience is dependent on signaling by the cytokine IL-10, highlighting a critical diet-microbiome-immune axis that promotes ENS resilience following SCI. Overall, we demonstrate that diet and microbially-derived signals distinctly impact recovery of the ENS after traumatic spinal injury. This protective diet-microbiome-immune axis may represent a foundation to uncover etiological mechanisms and future therapeutics for SCI-induced neurogenic bowel.

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Section: Introductionmentioning

confidence: 99%

“…Emerging data highlight an association between the gut microbiome and locomotor recovery or pain after SCI [24][25][26] . However, the potential pathogenicity of the injury-associated microbiome and precise contributions to recovery are unknown.…”

Section: Introductionmentioning

confidence: 99%

Diet-microbiome interactions promote enteric nervous system resilience following spinal cord injury

Hamilton,

Blackmer-Raynolds,

et al. 2024

Preprint

View full text Add to dashboard Cite

show abstract

Diet-microbiome interactions promote enteric nervous system resilience following spinal cord injury

Hamilton,

Blackmer-Raynolds,

et al. 2024

npj Biofilms Microbiomes

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Spinal cord injury (SCI) results in numerous systemic dysfunctions, including intestinal dysmotility and enteric nervous system (ENS) atrophy. The ENS has capacity to recover following perturbation, yet intestinal pathologies persist. With emerging evidence demonstrating SCI-induced alterations to gut microbiome composition, we hypothesized that microbiome modulation contributes to post-injury enteric recovery. Here, we show that intervention with the dietary fiber, inulin, prevents SCI-induced ENS atrophy and dysmotility in mice. While SCI-associated microbiomes and specific injury-sensitive gut microbes are not sufficient to modulate intestinal dysmotility after injury, intervention with microbially-derived short-chain fatty acid (SCFA) metabolites prevents ENS dysfunctions in injured mice. Notably, inulin-mediated resilience is dependent on IL-10 signaling, highlighting a critical diet-microbiome-immune axis that promotes ENS resilience post-injury. Overall, we demonstrate that diet and microbially-derived signals distinctly impact ENS survival after traumatic spinal injury and represent a foundation to uncover etiological mechanisms and future therapeutics for SCI-induced neurogenic bowel.

show abstract

Spinal cord injury-induced neurogenic bowel: A role for host-microbiome interactions in bowel pain and dysfunction

Cited by 2 publications

References 93 publications

Diet-microbiome interactions promote enteric nervous system resilience following spinal cord injury

Diet-microbiome interactions promote enteric nervous system resilience following spinal cord injury

Diet-microbiome interactions promote enteric nervous system resilience following spinal cord injury

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