WT and PAI-1−/− S. pneumoniae infected mice demonstrated significant increases in KC, IL-4, IL-5, IL-6, IL-10, IL-12, MCP-1, G-CSF and MIP-1β (Fig. 9, P < 0.05) compared to the saline controls.
Furthermore, the in vivo experimental metastasis assay conducted on C57BL/6 mice demonstrated significant activity of EIDLV-conjugated micelles in the reduction of pulmonary metastatic nodule formation in both pretreatment and post-treatment methods.
While infected PAI-1−/− mice demonstrated significant changes in lung volume (p = 0.02) by 3 days (Fig. 8a), trends in infected WT mice did not reach significance by 3 days.
PLs from saline and S. pneumoniae-infected WT and PAI-1−/− mice demonstrated significant increases in KC, IL-4, IL-5, IL-6, IL-10, IL-12, MCP-1, G-CSF, and MIP-1β * denotes P < 0.05, n = 4 7 mice/group).
In contrast, mast cells from Tnf−/− and Il6−/− mice demonstrated significant reduction in the ability to enhance neutrophil adhesion.
Wild-type mice demonstrated significant positive staining with SMI-31, reflecting a healthy axonal phenotype (Fig. 7A).
Twelve hours after immunisation WT mice demonstrate significant expansion of the lung nuocyte and basophil populations, correlating with detection of IL-33 in the BAL, whereas these cells failed to expand in the IL-33-deficient mice.
More recently a study using DCIR−/− mice also demonstrated significant survival compared with wild-type controls.
Using FcαRI transgenic mice, we demonstrated significant in vivo anti-tumour activity of IgA2 EGFR against A431 cells in peritoneal and lung xenograft models, as well as against B16F10-EGFR cells in a lung metastasis model in immunocompetent mice.
The neuron-specific Tsc1 mouse model demonstrated significant hypomyelination (37).
As a consequence of CB deficiency in the brains of Tg mice, we first demonstrated significant alterations in cell death pathways, synaptic transmission and MAPK signaling pathways from our initial antibody array analysis (Table 1).
