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LPS promotes CB3-induced myocarditis in resistant B10.A mice
J R Lane1, D A Neumann, A Lafond-Walker
1Johns Hopkins University, School of Hygiene and Public Health, Department of Immunology and Infectious Diseases, Baltimore, Maryland 21205.
Cellular Immunology
|August 1, 1991
Summary
Lipopolysaccharide (LPS) treatment can induce autoimmune myocarditis in Coxsackie virus B3 (CB3)-infected resistant mice. This suggests LPS modulates factors contributing to CB3-induced heart disease susceptibility.
Area of Science:
- Immunology
- Virology
- Cardiology
Background:
- Coxsackie virus B3 (CB3) infection causes autoimmune myocarditis in susceptible mice.
- Congenic mice (C57BL/10) are resistant to CB3-induced autoimmune myocarditis.
- Lipopolysaccharide (LPS) is an immunomodulator with potential to influence disease susceptibility.
Purpose of the Study:
- To investigate if LPS treatment alters susceptibility to CB3-induced autoimmune myocarditis in resistant mice.
- To characterize the immunological and pathological features of CB3-infected/LPS-treated mice.
Main Methods:
- Resistant B10.A mice were infected with CB3 and treated with LPS.
- Disease severity was assessed by mortality, immunoglobulin deposition, and cellular infiltration.
- Immunohistochemistry and Western immunoblotting were used to detect autoantibodies and antigens.
Main Results:
- CB3-infected/LPS-treated mice developed autoimmune myocarditis, similar to susceptible strains.
- Significant mortality, IgG deposition in the heart, and mononuclear cell infiltration were observed by Day 14.
- Serum IgG autoantibodies reactive with cardiac antigens were detected.
Conclusions:
- LPS treatment can induce autoimmune myocarditis in CB3-infected resistant mice.
- Increased cytokine levels and MHC expression in heart tissue due to LPS may contribute to disease susceptibility.
- This study highlights the role of immunomodulation in viral-induced autoimmune heart disease.