MIP-1 alpha mutant (-/-) mice were resistant to Coxsackievirus-induced myocarditis and had reduced pneumonitis but delayed viral clearance after influenza infection compared to wild-type mice.
Does disruption of the MIP-1 alpha gene reduce viral-induced inflammation in mice?
MIP-1 alpha is an important mediator of virus-induced inflammation in vivo, including Coxsackievirus-induced myocarditis.
Macrophage inflammatory protein-1 alpha (MIP-1 alpha) is a chemokine that has pro-inflammatory and stem cell inhibitory activities in vitro. Its biologic role in vivo was examined in mice in which the gene encoding MIP-1 alpha had been disrupted. Homozygous MIP-1 alpha mutant (-/-) mice were resistant to Coxsackievirus-induced myocarditis seen in infected wild-type (+/+) mice. Influenza virus-infected -/- mice had reduced pneumonitis and delayed clearance of the virus compared with infected +/+ mice. The -/- mice had no overt hematopoietic abnormalities. These results demonstrate that MIP-1 alpha is an important mediator of virus-induced inflammation in vivo.
Cook et al. (Fri,) conducted a other in Viral infection (Coxsackievirus and Influenza). MIP-1 alpha gene disruption vs. Wild-type (+/+) mice was evaluated on Coxsackievirus-induced myocarditis, influenza-induced pneumonitis, and viral clearance. MIP-1 alpha mutant (-/-) mice were resistant to Coxsackievirus-induced myocarditis and had reduced pneumonitis but delayed viral clearance after influenza infection compared to wild-type mice.
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