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Spinal Cord Injury and the Gut Microbiome: Mechanisms and Therapies for Bowel Dysfunction
Author(s) -
Jeffrey Elisabeth,
O'Connor Greg,
Deo Sapna,
Dietrich Dalton,
Daunert Sylvia
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb206
Subject(s) - microbiome , gut flora , immunology , spinal cord injury , gastrointestinal tract , gut–brain axis , dysbiosis , inflammation , biology , medicine , bioinformatics , neuroscience , spinal cord
Both experimental and clinical studies have shown that Spinal Cord Injury (SCI) has detrimental effects on remote organs and systems, yet there have been limited studies focusing on these more widespread effects. Despite attention to the pathophysiology of SCI with a goal of protection and repair, there is very little known about these gastrointestinal side‐effects or their effect on the gut microbiome. We sought to characterize long term effects of SCI on the gut by identifying changes in bacterial communication, microbiome composition, and inflammation. Bacterial quorum sensing molecules (QSMs) regulate various communication processes including growth, biofilm formation, and virulence factor production, thus providing information on the state of gut microbiota. Despite a repeatedly observed link between the intestinal microbiome and health, there is very limited data characterizing the gut microbiome in adult SCI patients with bowel dysfunction. We have employed a SCI rat model to investigate changes in the intestinal microbiome and gastrointestinal tract which may potentially contribute to or cause the GI dysfunction experienced by patients with SCI. Specifically, we determined the changes in the intestinal microbiota post‐SCI, most notably there was a significant increase in the relative abundance of Bifidobacteriaceae and Clostridiaceae post‐SCI, and investigated the potential underlying mechanisms via levels of pro‐inflammatory cytokines (IL1‐β, IL‐12, MIP‐2, and TNF‐α) and QSMs. This study continues to provide new information regarding the injury‐dependent changes on the gut microbiome and revealing microbiome‐host interactions that may contribute to the long term effects of SCI on the GI tract function. Identifying mechanisms behind these changes will aid in the development of new therapeutic strategies such as dietary modulation to improve quality of life for people living with SCI. Support or Funding Information University of Miami Miller School of Medicine, Miami Project to Cure Paralysis, Department of Biochemistry and Molecular Biology