ArticleBrain research2020
Depletion of gut microbiota is associated with improved neurologic outcome following traumatic brain injury.
Article in Brain research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 54 citations in OpenAlex.
- Aging-caused the changes of the gut microbiota drive intestinal barrier dysfunction and increase sepsis susceptibility.Gut microbes · 2026Article
- Improving the Outcome of Brain-Injured Patients by Non-Continuous Feeding to Prevent Dysbiosis.Nutrients · 2026Review
- Gastrointestinal Dysfunction in Critically Ill Patients With Traumatic Brain Injury: Clinical Implications and Putative Mechanisms: a Narrative Review.Current neurology and neuroscience reports · 2026Review
- Mild concussion impairs extinction of avoidance and alters respective brain circuits in male rats.Experimental neurology · 2026Article
- Circulating Short-Chain Fatty Acid Profile Predicts Functional Outcome After Moderate-to-Severe Traumatic Brain Injury.Critical care explorations · 2026Article
- Antibiotic-induced gut microbiome remodeling reduces neuroinflammation in traumatic brain injury.Communications biology · 2026Article
- Therapeutic potential ofMicrobiome research reports · 2026Article
- The Gut Microbiome as a Modulator of Traumatic Brain Injury Pathology and Symptoms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Review
- Gut microbiome remodeling by antibiotics reduces neuroinflammation in traumatic brain injury.Research square · 2025Article
- Partially hydrolyzed guar gum alleviates neurological deficits and gastrointestinal dysfunction in mice with traumatic brain injury.Neurosurgical review · 2025Article
- Chitosan lactate improves repeated closed head injury-generated motor and neurological dysfunctions in mice by impacting microbiota gut-brain axis.Metabolic brain disease · 2025Article
- Growth Differentiation Factor-15 Knockout Mice Are Protected from Neonatal Hypoxic-Ischemic Injury in a Sex-Dependent Manner.Developmental neuroscience · 2025Article
- Radiation-Induced Brain Injury: Mechanistic Insights and the Promise of Gut-Brain Axis Therapies.Brain sciences · 2024Review
- New insights into metabolism dysregulation after TBI.Journal of neuroinflammation · 2024Review
- Antibiotic treatment induces microbiome dysbiosis and reduction of neuroinflammation following traumatic brain injury in mice.Research square · 2024Article
- Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies.Journal of neuroinflammation · 2024Review
- Article
- Temporal shifts to the gut microbiome associated with cognitive dysfunction following high-fat diet consumption in a juvenile model of traumatic brain injury.Physiological genomics · 2024Article
- Current state of neuroprotective therapy using antibiotics in human traumatic brain injury and animal models.BMC neuroscience · 2024Review
- Acute gastrointestinal permeability after traumatic brain injury in mice precedes a bloom in Akkermansia muciniphila supported by intestinal hypoxia.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Signaling between intestinal microbiota and the brain influences neurologic outcome in multiple forms of brain injury. The impact of gut microbiota following traumatic brain injury (TBI) has not been well established. Our objective was to compare TBI outcomes in specific pathogen-free mice with or without depletion of intestinal bacteria. Adult male C57BL6/J SPF mice (n = 6/group) were randomized to standard drinking water or ampicillin (1 g/L), metronidazole (1 g/L), neomycin (1 g/L), and vancomycin (0.5 g/L) (AMNV) containing drinking water 14 days prior to controlled cortical impact (CCI) model of TBI. 16S rRNA gene sequencing of fecal pellets was performed and alpha and beta diversity determined. Hippocampal neuronal density and microglial activation was assessed 72 h post-injury by immunohistochemistry. In addition, mice (n = 8-12/group) were randomized to AMNV or no treatment initiated immediately after CCI and memory acquisition (fear conditioning) and lesion volume assessed. Mice receiving AMNV had significantly reduced alpha diversity (p < 0.05) and altered microbiota community composition compared to untreated mice (PERMANOVA: p < 0.01). Mice receiving AMNV prior to TBI had increased CA1 hippocampal neuronal density (15.2 ± 1.4 vs. 8.8 ± 2.1 cells/0.1 mm; p < 0.05) and a 26.6 ± 6.6% reduction in Iba-1 positive cells (p < 0.05) at 72 h. Mice randomized to AMNV immediately after CCI had attenuated associative learning deficit on fear conditioning test (%freeze Cue: 63.7 ± 2.7% vs. 41.0 ± 5.1%, p < 0.05) and decreased lesion volume (27.2 ± 0.8 vs. 24.6 ± 0.7 mm
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.