Analysis Tools
immune system
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• unchallenged mice show normal immunocyte development with no differences in the proportion and number of T cells, B cells, macrophages or neutrophils in different tissues and blood relative to wild-type controls
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• in vitro, peritoneal macrophages (PMs) and bone marrow-derived macrophages (BMDMs) show significantly higher mRNA and protein levels of TNF and IL-6 in response to LPS (100 ng/ml) challenge
• BMDMs show marked up-regulation of CD80, CD86 and MHC-II protein after LPS treatment (100 ng/ml) for 24 h, indicating macrophage over-activation
• LPS-treated PMs show enhanced expression of inducible nitric oxide synthase (iNOS, an M1 polarization marker) and higher mRNA levels of Nos2, indicating LPS-mediated polarization towards the M1 inflammatory phenotype
• LPS-treated PMs show significantly higher levels of phosphorylated p38 MAPK, extracellular signal regulated kinase (ERK), JUN N-terminal kinase (JNK) and NF-kappaB p65, indicating increased activation of the MAPK and NF-kappaB signaling pathways
• pretreatment of PMs with PD98059 (an MEK1/2 inhibitor) or JSH23 (an NF-kappaB inhibitor) prior to LPS challenge significantly reduces LPS-induced Tnf, Il6, and Ifnb1 mRNA levels, as in wild-type PMs
• BMDMs show normal expression of CD206 (a marker of M2 macrophages) after treatment with IL-4 (10 ng/ml) for 24 h; similarly, IL-4-treated PMs show normal expression of Arg1 (an M2 polarization marker), suggesting that M2 macrophages are unaffected
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show significantly higher serum levels of IFN-beta protein than wild-type controls
• however, when mice are i.v. pre-injected with clodronate liposomes for 48 h (to induce macrophage depletion) and then challenged by LPS (5 mg/kg) for 2 h, serum IFN-beta levels are significantly reduced to levels seen in similarly treated wild-type controls
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show significantly higher serum levels of IL-6 than wild-type controls
• 12 h after cecal ligation and puncture (CLP), mice show significantly higher serum levels of IL-6 than wild-type controls
• however, when mice are i.v. injected with clodronate liposomes for 48 h (to induce macrophage depletion) and then challenged by LPS (5 mg/kg) for 2 h, serum IL-6 levels are significantly reduced to levels seen in similarly treated wild-type controls
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show significantly higher serum levels of TNF than wild-type controls
• 12 h after CLP, mice show significantly higher serum levels of TNF than wild-type controls
• however, when mice are i.v. injected with clodronate liposomes for 48 h (to induce macrophage depletion) and then challenged by LPS (5 mg/kg) for 2 h, serum TNF levels are significantly reduced to levels seen in similarly treated wild-type controls
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• in vitro, peritoneal macrophages (PMs) and bone marrow-derived macrophages (BMDMs) produce significantly higher levels of IL-6 protein than wild-type cells in response to LPS (100 ng/ml), along with increased Il6 mRNA levels at various time-points after LPS challenge
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• in vitro, PMs and BMDMs produce significantly higher levels of TNF protein than wild-type cells in response to LPS (100 ng/ml), along with increased Tnf mRNA levels at various time-points after LPS challenge
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show markedly higher serum levels of inflammatory factors (TNF, IL-6 and IFN-beta protein) than wild-type controls; after LPS (10 mg/kg) challenge for 18 h, inflammatory cell infiltration, hemorrhage, interstitial pneumonitis, and the number of Ly6G+ cells in lung are significantly higher than in controls
• nearly all mice i.p. injected with a lethal LPS dose (15 mg/kg) die at 50 h post-injection
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homeostasis/metabolism
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show significantly higher serum levels of IFN-beta protein than wild-type controls
• however, when mice are i.v. pre-injected with clodronate liposomes for 48 h (to induce macrophage depletion) and then challenged by LPS (5 mg/kg) for 2 h, serum IFN-beta levels are significantly reduced to levels seen in similarly treated wild-type controls
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show significantly higher serum levels of IL-6 than wild-type controls
• 12 h after cecal ligation and puncture (CLP), mice show significantly higher serum levels of IL-6 than wild-type controls
• however, when mice are i.v. injected with clodronate liposomes for 48 h (to induce macrophage depletion) and then challenged by LPS (5 mg/kg) for 2 h, serum IL-6 levels are significantly reduced to levels seen in similarly treated wild-type controls
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• mice i.p. injected with LPS (5 mg/kg) for 2 h show significantly higher serum levels of TNF than wild-type controls
• 12 h after CLP, mice show significantly higher serum levels of TNF than wild-type controls
• however, when mice are i.v. injected with clodronate liposomes for 48 h (to induce macrophage depletion) and then challenged by LPS (5 mg/kg) for 2 h, serum TNF levels are significantly reduced to levels seen in similarly treated wild-type controls
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• ~50% of mice die at 40 h after cecal ligation and puncture (CLP) and only 20% are alive at 7 days after CLP surgery; in contrast, all wild-type controls are alive at 40 h and ~50% survive 7 days after CLP
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• 24 h after CLP surgery, mice show more severe lung injury and decreased survival relative to wild-type controls
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mortality/aging
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• ~50% of mice die at 40 h after cecal ligation and puncture (CLP) and only 20% are alive at 7 days after CLP surgery; in contrast, all wild-type controls are alive at 40 h and ~50% survive 7 days after CLP
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• nearly all mice i.p. injected with a lethal LPS dose (15 mg/kg) die at 50 h post-injection; in contrast, 80% of wild-type controls are still alive at 50 h with ~60% surviving 100 h after LPS challenge
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hematopoietic system
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• in vitro, peritoneal macrophages (PMs) and bone marrow-derived macrophages (BMDMs) show significantly higher mRNA and protein levels of TNF and IL-6 in response to LPS (100 ng/ml) challenge
• BMDMs show marked up-regulation of CD80, CD86 and MHC-II protein after LPS treatment (100 ng/ml) for 24 h, indicating macrophage over-activation
• LPS-treated PMs show enhanced expression of inducible nitric oxide synthase (iNOS, an M1 polarization marker) and higher mRNA levels of Nos2, indicating LPS-mediated polarization towards the M1 inflammatory phenotype
• LPS-treated PMs show significantly higher levels of phosphorylated p38 MAPK, extracellular signal regulated kinase (ERK), JUN N-terminal kinase (JNK) and NF-kappaB p65, indicating increased activation of the MAPK and NF-kappaB signaling pathways
• pretreatment of PMs with PD98059 (an MEK1/2 inhibitor) or JSH23 (an NF-kappaB inhibitor) prior to LPS challenge significantly reduces LPS-induced Tnf, Il6, and Ifnb1 mRNA levels, as in wild-type PMs
• BMDMs show normal expression of CD206 (a marker of M2 macrophages) after treatment with IL-4 (10 ng/ml) for 24 h; similarly, IL-4-treated PMs show normal expression of Arg1 (an M2 polarization marker), suggesting that M2 macrophages are unaffected
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