Adoption of Exhaust Air Dust Testing in SPF Rodent Facilities.

Reliable detection of unwanted microbial agents is essential for meaningful health monitoring in laboratory animal facilities. Most rodents at our institution are housed in IVC rack systems to minimize aerogenic transmission of infectious agents between cages. The most commonly used rodent health monitoring systems expose live sentinel rodents to soiled bedding collected from other rodent cages on IVC racks and subsequently test these soiled-bedding sentinels for evidence of infection with excluded agents.

Effect of Chronic Vitamin D Deficiency on the Development and Severity of DSS-Induced Colon Cancer in Mice.

Both human epidemiologic data and animal studies suggest that low serum vitamin D increases the risk of inflammatory bowel disease (IBD) and consequently IBD-associated colorectal cancer. We tested the hypothesis that vitamin D deficiency increases the risk for colitis-associated colon cancer (CAC) by using an established CAC mouse model, 129-/J () mice, which have defective transforming growth factor β-signaling and develop colitis and CAC after the administration of dextran sodium sulfate (DSS). After determining a dietary regimen that induced chronic vitamin D deficiency in mice, we assessed the effects of vitamin D deficiency on CAC.

Lack of Effect of Murine Norovirus Infection on the CD4 CD45RB T-cell Adoptive Transfer Mouse Model of Inflammatory Bowel Disease.

Murine norovirus (MNV) infection is highly prevalent in laboratory mice. Although MNV infection does not typically induce clinical disease in most laboratory mice, infection may nonetheless affect mouse models of disease by altering immune responses. We previously reported that MNV altered the bacterial-induced mouse model of inflammatory bowel disease (IBD) using -infected mice.

Validation studies for germ-free mice as a bio-assay to test the causative role of fecal microbiomes in IBD.

While the association between microbiomes and inflammatory bowel disease (IBD) is well known, establishing causal relationships between the two is difficult in humans. Germ-free (GF) mice genetically susceptible to IBD can address this question. mice with defective transforming growth factor ß signaling are a model of IBD and colon cancer.