The innate immune response to coxsackievirus B3 predicts progression to cardiovascular disease and heart failure in male mice
2011

Immune Response to Coxsackievirus B3 and Heart Disease in Male Mice

Sample size: 10 publication 10 minutes Evidence: moderate

Author Information

Author(s): Onyimba Jennifer A, Coronado Michael J, Garton Amanda E, Kim Joseph B, Bucek Adriana, Bedja Djahida, Gabrielson Kathleen L, Guilarte Tomas R, Fairweather DeLisa

Primary Institution: Johns Hopkins University

Hypothesis

Sex differences in innate immune genes in the spleen would uncover pathways that are important in the susceptibility to acute myocarditis and dilated cardiomyopathy.

Conclusion

Male mice had a greater splenic expression of genes associated with cholesterol metabolism and activation of the androgen receptor compared to females, which may drive increased inflammation and heart disease.

Supporting Evidence

  • Male mice showed higher splenic expression of genes regulating cholesterol metabolism compared to females.
  • Infected males had decreased levels of the androgen receptor, indicating receptor activation.
  • The study identified significant gene changes in males that were not due to increased viral replication.

Takeaway

This study found that male mice respond differently to a virus that can cause heart disease, showing more signs of inflammation and changes in certain genes than female mice.

Methodology

Male and female BALB/c mice were infected with coxsackievirus B3, and their spleens were analyzed for gene expression 12 hours post-infection using microarray analysis.

Potential Biases

Potential bias in gene expression analysis due to not correcting for multiple comparisons.

Limitations

The study primarily focused on male mice, and findings may not be directly applicable to females or other species.

Participant Demographics

Male and female BALB/c mice, aged 8 to 10 weeks.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1186/2042-6410-2-2

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