Cost and Effectiveness of Commercially Available Nesting Substrates for Deer Mice (Peromyscus maniculatus).

Provision of nesting material promotes species-typical behaviors in rodents including deer mice (Peromyscus maniculatus). The purpose of this study was to determine which commercially available nesting material best promotes complex nest building in the subspecies P. m. bairdii yet remains cost-effective for use as enrichment in a laboratory research setting. An existing breeding colony consisting of cages containing all male mice, all female mice, and breeding pairs was evaluated. Five commercially available substrates-compressed cotton squares, cylindrical compressed cotton, cellulose bedding containing small pieces of evenly dispersed compressed paper, brown crinkled paper, and white crinkled paper-were provided according to the manufacturer's recommendation. Nests were evaluated at 24 h after cage change and scored for complexity. Nest complexity was compared between breeding pairs and single-sex cages and between male and female mice. Cages housing breeding pairs with pups had the highest average complexity score. The dispersed paper substrate was the least expensive substrate tested but had the lowest average nest complexity score. Nesting scores for brown crinkled paper, compressed cotton squares, and compressed cotton cylinders did not differ significantly despite the range in cost. Brown crinkled paper was the second least-expensive substrate tested, and mice used it to build consistently complex nests, making it the most practical substrate for use as enrichment for deer mice in a laboratory setting.

Thrombospondin-1 contributes to mortality in murine sepsis through effects on innate immunity.

BACKGROUND: Thrombospondin-1 (TSP-1) is involved in many biological processes, including immune and tissue injury response, but its role in sepsis is unknown. Cell surface expression of TSP-1 on platelets is increased in sepsis and could activate the anti-inflammatory cytokine transforming growth factor beta (TGFß1) affecting outcome. Because of these observations we sought to determine the importance of TSP-1 in sepsis. METHODOLOGY/PRINCIPAL FINDINGS: We performed studies on TSP-1 null and wild type (WT) C57BL/6J mice to determine the importance of TSP-1 in sepsis. We utilized the cecal ligation puncture (CLP) and intraperitoneal E. coli injection (i.p. E. coli) models of peritoneal sepsis. Additionally, bone-marrow-derived macrophages (BMMs) were used to determine phagocytic activity. TSP-1-/- animals experienced lower mortality than WT mice after CLP. Tissue and peritoneal lavage TGFß1 levels were unchanged between animals of each genotype. In addition, there is no difference between the levels of major innate cytokines between the two groups of animals. PLF from WT mice contained a greater bacterial load than TSP-1-/- mice after CLP. The survival advantage for TSP-1-/- animals persisted when i.p. E. coli injections were performed. TSP-1-/- BMMs had increased phagocytic capacity compared to WT. CONCLUSIONS: TSP-1 deficiency was protective in two murine models of peritoneal sepsis, independent of TGFß1 activation. Our studies suggest TSP-1 expression is associated with decreased phagocytosis and possibly bacterial clearance, leading to increased peritoneal inflammation and mortality in WT mice. These data support the contention that TSP-1 should be more fully explored in the human condition.