Identifying Genes Linking Inflammation to Atherosclerosis
Author Information
Author(s): Sivapalaratnam Suthesh, Farrugia Rosienne, Nieuwdorp Max, Langford Cordelia F, van Beem Rachel T, Maiwald Stephanie, Zwaginga Jaap Jan, Gusnanto Arief, Watkins Nicholas A, Trip Mieke D, Ouwehand Willem H
Primary Institution: Academic Medical Center, Amsterdam, The Netherlands
Hypothesis
Endotoxin exposure in vivo results in changes in monocyte transcriptome that could lead to a more atherogenic phenotype.
Conclusion
In vivo endotoxin exposure of healthy individuals resulted in the identification of several candidate genes through which systemic inflammation links to atherosclerosis.
Supporting Evidence
- All subjects who received LPS experienced the anticipated clinical response indicating successful stimulation.
- 11 genes were identified as being differentially expressed one hour after LPS infusion.
- 28 genes were identified as being differentially expressed four hours after LPS infusion.
- Comparison with in vitro data led to the identification of 6 strong candidate genes.
Takeaway
The study looked at how a substance from bacteria affects certain blood cells in healthy people, helping us understand how inflammation might lead to heart problems.
Methodology
Healthy volunteers were infused with lipopolysaccharide (LPS) to mimic systemic inflammation, and monocyte RNA was analyzed for gene expression changes.
Potential Biases
Potential bias due to the small number of participants and the specific inclusion criteria.
Limitations
The study had a small sample size and the results may not fully represent the entire population of monocytes due to their migration into the vessel wall.
Participant Demographics
16 healthy Caucasian male volunteers with an average age of 23.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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