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August 1, 1991Cellular ImmunologyOpen Access

LPS promotes CB3-induced myocarditis in resistant B10.A mice

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Why the study?

Does LPS treatment promote CB3-induced autoimmune myocarditis in genetically resistant B10.A mice?

Population

B10.A mice (a strain normally resistant to Coxsackie virus B3-induced autoimmune myocarditis)

Comparison

Coxsackie virus B3 infection combined with… vs Mice infected only with CB3 or treated only with…

Design

Preclinical

Follow-up

14 days

Authors

JLJames R. LaneNational Institutes of HealthDNDavid A. NeumannJohns Hopkins UniversityALAnne Lafond-WalkerJohns Hopkins University

Discussion

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Implication

Suggests LPS overcomes genetic resistance in murine myocarditis models; leaves open cytokine/MHC roles in human susceptibility.

Structured PICO

Does LPS treatment promote CB3-induced autoimmune myocarditis in genetically resistant B10.A mice?

P
Population
B10.A mice (a strain normally resistant to Coxsackie virus B3-induced autoimmune myocarditis)
I
Intervention
Coxsackie virus B3 (CB3) infection combined with lipopolysaccharide (LPS) treatment
C
Comparator
Mice infected only with CB3 or treated only with LPS
O
Outcome
Development of autoimmune myocarditis (assessed by mortality, myocardial immunoglobulin deposition, and mononuclear cell infiltration)surrogate

LPS treatment overcomes genetic resistance to CB3-induced autoimmune myocarditis in B10.A mice, suggesting a role for cytokines and MHC expression in disease susceptibility.

Cite This Study

Lane et al. (1991) studied this question.

synapsesocial.com/papers/6a71a48ca528af2d65c42879https://doi.org/10.1016/0008-8749(91)90396-s

Topics

Myocarditis
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