Decontamination of a barrier facility using microisolator cages and provisional partitioning.

In 2000, the authors found endemic infections of mouse hepatitis virus, minute virus of mice, Syphacia obvelata, and Myobia musculi among mice in a large barrier facility at the University of Mainz. To eliminate the infections, they subdivided the facility into two distinct hygiene units. However, architectural constraints made it impossible to completely separate the HVAC systems of both hygiene units and to establish adequate personnel locks. To compensate for these suboptimal barrier conditions of the two newly established units, the authors replaced the open-top caging and open-servicing system with filter-top cages that were manipulated in cage-changing stations. The authors then depopulated the two units in series, independently eliminating the contaminated mice and restocking the units with SPF animals. In spite of the high infection pressure and the suboptimal barrier conditions, the authors had only a single case of recontamination.

Interferon-gamma induces chronic active myocarditis and cardiomyopathy in transgenic mice.

Chronic heart failure is associated with an activation of the immune system characterized among other factors by the cardiac synthesis and serum expression of proinflammatory cytokines. There is unequivocal clinical and experimental evidence that the cytokine tumor necrosis factor-alpha is involved in the development of chronic heart failure, but a putative cardiotoxic potential of the proinflammatory cytokine interferon (IFN)-gamma remains primarily unknown. To investigate this issue we analyzed the cardiac phenotype of SAP-IFN-gamma transgenic mice, which constitutively express IFN-gamma in their livers and hence exhibit high circulating serum levels of this cytokine. SAP-IFN-gamma mice spontaneously developed chronic active myocarditis, characterized by the infiltration of not only CD4(+) and CD8(+) T cells but also Mac2(+) (galectin 3(+)) macrophages and CD11c(+) dendritic cells, eventually culminating in cardiomyopathy. Echocardiographic analyses exhibited a left ventricular dilation and impaired systolic function induced by IFN-gamma overexpression. IFN-gamma-mediated cardiotoxicity was associated with high-level cardiac transcription of the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-12 and the macrophage-attracting chemokines MCP1 and MIP1-alpha. Myotoxic IFN-gamma effects could not be detected in smooth or striated muscle tissue, suggesting cardiomyocellular specificity of the toxic IFN-gamma effect. The precise mechanism of IFN-gamma cardiotoxicity remains to be elucidated.