Analysis Tools
immune system
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• mutant mice have normal numbers of basophils in the bone marrow, spleen and peripheral blood, as well as normal numbers of mast cells in the ear skin and peritoneum relative to wild-type controls
• after stimulation with anti-TNP IgE plus TNP-OVA, mutant bone marrow-derived basophils (BMBAs) degranulate and produce IL-4 and IL-6 to a similar extent as wild-type BMBAs
• IgE-dependent passive cutaneous anaphylaxis (PCA) is normal, with no differences in the extent of microvascular leakage or mast cell-dependent, immediate-type ear swelling relative to wild-type controls
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• mutant mice sensitized with TNP-specific IgE and challenged with an intradermal injection of TNP-OVA in ear skin show ameliorated IgE-mediated chronic allergic inflammation (IgE-CAI), with a ~50% decrease in ear swelling on day 4 post-challenge and significantly reduced microvascular permeability and leukocyte infiltration in the skin lesion relative to wild-type controls
• 3 days after IgE-CAI induction, both the number of total cells and CD45+ hematopoietic cells are reduced to <50% that in wild-type controls, with significantly lower numbers of basophils, eosinophils, neutrophils, and monocytes/macrophages infiltrating the skin lesion
• treatment with a COX-2 inhibitor (meloxicam or celecoxib) fails to attenuate IgE-CAI ear swelling in mutant mice, unlike in similarly treated wild-type controls
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cardiovascular system
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• 3 days after IgE-CAI induction with TNP-OVA, mutant mice show a significantly lower increase in microvascular permeability in the skin lesion relative to wild-type controls, as measured by Evans blue dye leakage
• whereas IgE-CAI vascular permeability is suppressed by treatment with meloxicam (COX-2 inhibitor) but not SC560 (COX-1 inhibitor) in wild-type mice, neither drug has a significant effect in mutant mice
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cellular
| N |
• in a transwell migration assay, mutant BMBAs exhibit normal migration ability in response to chemokine MIP-2
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