Analysis Tools
homeostasis/metabolism
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• mouse embryonic fibroblasts (MEFs) fail to form autophagosomes when deprived of nutrients
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• MEFs fail to form autophagosomes when deprived of nutrients
• degradation of long lived proteins in MEFs is reduced by about a third
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mortality/aging
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• neonates die within one day of delivery due to an inability to survive neonatal starvation
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cellular
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• mouse embryonic fibroblasts (MEFs) fail to form autophagosomes when deprived of nutrients
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• MEFs fail to form autophagosomes when deprived of nutrients
• degradation of long lived proteins in MEFs is reduced by about a third
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immune system
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• irradiated wild-type mice that have received mutant fetal liver cells to replace all haematopoietic cells are highly susceptible to dextran sulfate sodium (DSS)-induced colitis
• five days after DSS treatment, all mice die of an inflammatory bowel disease compared to controls that all live
• severe inflammation in the colon results from the DSS treatment with larger areas of ulceration and increased infiltration of lymphocytes
• body weight loss is more severe with mice losing 25% of their bodyweight before dying
• levels of IL-1beta and IL-18 are elevated in the sera of mice with 4 days of DSS treatment
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• IL-1beta production by fetal-derived or chimeric-derived macrophages is enhanced to TLR3, TLR4, TLR7 and TLR9 ligands
• levels of reactive oxygen species is higher in fetal liver-derived macrophages than controls after stimulation with LPS
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• IL-1beta production by fetal-derived macrophages is highly elevated (6-10 fold) when stimulated with LPS or synthetic lipid A
• similar results are obtained from peritoneal or bone-marrow derived macrophages that are isolated from irradiated mice that have received mutant fetal liver cells
• higher augmentation of IL-1beta production by fetal-derived macrophages occurs with incubation of several different species of non-invasive Gram-negative bacteria
• IL-1beta production by fetal-derived macrophages is enhanced to a lesser degree by ligands for TLR3, TLR7 and TLR9
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• IL-18 secretion is enhanced in fetal-derived macrophages when stimulated with LPS
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digestive/alimentary system
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• irradiated wild-type mice that have received mutant fetal liver cells to replace all haematopoietic cells are highly susceptible to dextran sulfate sodium (DSS)-induced colitis
• five days after DSS treatment, all mice die of an inflammatory bowel disease compared to controls that all live
• severe inflammation in the colon results from the DSS treatment with larger areas of ulceration and increased infiltration of lymphocytes
• body weight loss is more severe with mice losing 25% of their bodyweight before dying
• levels of IL-1beta and IL-18 are elevated in the sera of mice with 4 days of DSS treatment
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hematopoietic system
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• IL-1beta production by fetal-derived or chimeric-derived macrophages is enhanced to TLR3, TLR4, TLR7 and TLR9 ligands
• levels of reactive oxygen species is higher in fetal liver-derived macrophages than controls after stimulation with LPS
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