RGD Reference Report - Acetate supplementation reduces microglia activation and brain interleukin-1beta levels in a rat model of Lyme neuroborreliosis. - Rat Genome Database

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Acetate supplementation reduces microglia activation and brain interleukin-1beta levels in a rat model of Lyme neuroborreliosis.

Authors: Brissette, CA  Houdek, HM  Floden, AM  Rosenberger, TA 
Citation: Brissette CA, etal., J Neuroinflammation. 2012 Nov 7;9:249. doi: 10.1186/1742-2094-9-249.
RGD ID: 7193053
Pubmed: PMID:23134838   (View Abstract at PubMed)
PMCID: PMC3520777   (View Article at PubMed Central)
DOI: DOI:10.1186/1742-2094-9-249   (Journal Full-text)

ABSTRACT: BACKGROUND: We have found that acetate supplementation significantly reduces neuroglia activation and pro-inflammatory cytokine release in a rat model of neuroinflammation induced with lipopolysaccharide. To test if the anti-inflammatory effect of acetate supplementation is specific to a TLR4-mediated injury, we measured markers of neuroglia activation in rats subjected to B. burgdorferi-induced neuroborreliosis that is mediated in large part by a TLR2-type mechanism. METHODS: In this study, rats were subjected to Lyme neuroborreliosis following an intravenous infusion of B. burgdorferi (B31-MI-16). Acetate supplementation was induced using glyceryl triacetate (6g/kg) by oral gavage. Immunohistochemistry, qPCR, and western blot analyses were used to measure bacterial invasion into the brain, neuroglial activation, and brain and circulating levels of interleukin 1beta. Statistical analysis was performed using one-way analysis of variance (ANOVA) followed by a Tukey's post hoc tests or using a Student's t test assuming unequal variances when appropriate. RESULTS: We found that acetate supplementation significantly reduced microglia activation by 2-fold as determined by immunohistochemical and western blot analysis. Further, acetate supplementation also reduced the expression of the pro-inflammatory cytokine IL-1beta by 2-fold as compared to controls. On the other hand, the inoculation of rats with B. burgdorferi had no effect on astroglial activation as determined by immunocytochemistry and western blot analysis despite significant increases in circulation levels of antigen toward B. burgdorferi and presence of the bacteria in the central nervous system. CONCLUSIONS: These results suggest that microglial activation is an essential component to neuroborreliosis and that acetate supplementation may be an effective treatment to reduce injury phenotype and possibly injury progression in Lyme neuroborreliosis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
IL1BHumanLyme Neuroborreliosis  ISOIl1b (Rattus norvegicus) RGD 
Il1bRatLyme Neuroborreliosis  IDA  RGD 
Il1bMouseLyme Neuroborreliosis  ISOIl1b (Rattus norvegicus) RGD 

Objects Annotated

Genes (Rattus norvegicus)
Il1b  (interleukin 1 beta)

Genes (Mus musculus)
Il1b  (interleukin 1 beta)

Genes (Homo sapiens)
IL1B  (interleukin 1 beta)


Additional Information