Analysis Tools
mortality/aging
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• poor survival (20%) after 30 minutes of ischemia while 70% partial hepatectomy performed
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• in mice infected with S. pneumoniae
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• caecal ligation and puncture (CLP) causes greater mortality in mutants than wild-type in the first 24 hours after CLP (100 vs 20% mortality)
• reconstitution of mice with ip. injection of purified human C3 (HuC3) reduces mortality from 100% to 40% in the first 24 hours
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immune system
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• secondary immune responses are similar in wild-type and mutant mice, so helper T cell function is normal
• B cells from deficient mice show normal proliferative effects in response to surface IgM crosslinking
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• after CLP less peritoneal mast cells can be recovered from Cr3-deficient mice compared to controls
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• 1 hour after CLP, 50% of peritoneal cells are neutrophils and after 3 hours, 90% are neutrophils while in C3-deficient mice, after 1 hour only 1% and 45% after 3 hours are neutrophils
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• bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls
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• after immunization, wild-type mice develop germinal centers (GC) in ~half of splenic follicles while ~10% of splenic follicles in C3-deficient mice contain GCs
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• diameter of GCs are less than that observed in wild-type
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• reduced levels at 6 and 24 hours after 6 and 24 hours of reperfusion
(J:152533)
• Il-6 production after vitamin D3 stimulation is significantly reduced
(J:166640)
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• levels of Tnfa in peritoneal lavage fluids are reduced in C3-deficient mice compared to controls at 1 hour (158 mg/pl vs 400 mg/pl) and 3 hours (218 mg/pl vs 663 pg/ml) after CLP
• treatment with HuC3 restores levels of Tnfa production in mutants to wild-type levels
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• reduced TNFalpha levels at 6 and 24 hours after 6 and 24 hours of reperfusion
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• in an in vitro assay, opsonization with serum from C3-deficient mice and 1% immune rabbit serum only resulted in a 0.2 log10 reduction in GBS CFU compared to a 1.0 log10 reduction by normal mouse serum
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• mast cells from mutants 1 or 3 hours after CLP show reduced degranulation compared to wild-type (75% of wild-type cells vs <50% of C3-deficient cells)
• treatment with HuC3 results in comparable levels of mast cell degranulation to wild-type
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• in response to immunization with bacteriophage (phiX174), a T cell dependent antigen, C3-deficient mice mount a weak Ig M response but fail to switch to IgG
• when immunized with a 10-fold higher amount of bacteriophage, mice show a weak IgG response but response is still 10-fold lower than wild-type
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• mild hepatitis is observed in a small number (1/11) of mice surviving systemic challenge with GBS doses of 102 to 105 CFU upon necropsy 15 days post-challenge; there are aggregates of mononuclear or polymorphonuclear leukocytes in hepatic sinusoids; wild-type animals that receive higher doses of GBS showed similar lesions
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• mice challenged with group B Streptococci (GBS) infection become bacteremic within 3 days and die or clear bacteria and survive; C3-deficient mice challenged with GBS infection showed a decreased LD50 dose compared to immunocompetent controls (LD50 dose: control 6.3 x 104 vs. 1.3 x 103 in C3-deficient mice)
(J:30152)
• increased mortality from GBS infection compared to controls is limited to the first 3 days after challenge
(J:30152)
• when pregnant dams are immunized with immune rabbit serum, pups are not protected against lethal challenge on day 2 of life (15/20 pups die within 48 hours)
(J:30152)
• at 1 or 3 hours after CLP, cytocentrifuge preparations or peritoneal fluid from C3-deficient mice have reduced neutrophil counts and large numbers of bacteria, compared to wild-type which have few or no bacteria
(J:44240)
• treatment with HuC3 restore neutrophil numbers and enhance bacterial clearance to wild-type levels
(J:44240)
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• in mice infected with S. pneumoniae
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cardiovascular system
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• upeon reperfusion of ischemic intestine (jejunum), permeability index (PI) of injured C3-deficient mice is reduced compared to control treated wild-type (PI of 2.25 vs 3.26 in controls)
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digestive/alimentary system
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• mice show less evidence of infarction compared to controls
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homeostasis/metabolism
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• after 70% partial hepatectomy
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• reduced levels at 6 and 24 hours after 6 and 24 hours of reperfusion
(J:152533)
• Il-6 production after vitamin D3 stimulation is significantly reduced
(J:166640)
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• lower levels of myeloperoxidase in livers at 6 and 24 hours of reperfusion
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• levels lower during reperfusion after ischemia than in controls
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• after 70% partial hepatectomy
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• levels of Tnfa in peritoneal lavage fluids are reduced in C3-deficient mice compared to controls at 1 hour (158 mg/pl vs 400 mg/pl) and 3 hours (218 mg/pl vs 663 pg/ml) after CLP
• treatment with HuC3 restores levels of Tnfa production in mutants to wild-type levels
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• reduced TNFalpha levels at 6 and 24 hours after 6 and 24 hours of reperfusion
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• mice are resistant to ischemia reperfusion-induced renal injury
• serum urea nitrogen is reduced 31% to 55% compared to wild-type mice subjected to ischemia reperfusion
• neutrophil infiltration at the site of injury was reduced
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hematopoietic system
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• after CLP less peritoneal mast cells can be recovered from Cr3-deficient mice compared to controls
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• 1 hour after CLP, 50% of peritoneal cells are neutrophils and after 3 hours, 90% are neutrophils while in C3-deficient mice, after 1 hour only 1% and 45% after 3 hours are neutrophils
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• bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls
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• after immunization, wild-type mice develop germinal centers (GC) in ~half of splenic follicles while ~10% of splenic follicles in C3-deficient mice contain GCs
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• diameter of GCs are less than that observed in wild-type
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• mast cells from mutants 1 or 3 hours after CLP show reduced degranulation compared to wild-type (75% of wild-type cells vs <50% of C3-deficient cells)
• treatment with HuC3 results in comparable levels of mast cell degranulation to wild-type
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liver/biliary system
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• histological evidence of injury after 6 and 24 hours of reperfusion following ischemia
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• after 70% partial hepatectomy
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• increased steatosis after 70% hepatectomy
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• impaired hepatocyte proliferation after 30 minutes of ischemia during 70% partial hepatectomy
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• mild hepatitis is observed in a small number (1/11) of mice surviving systemic challenge with GBS doses of 102 to 105 CFU upon necropsy 15 days post-challenge; there are aggregates of mononuclear or polymorphonuclear leukocytes in hepatic sinusoids; wild-type animals that receive higher doses of GBS showed similar lesions
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• significant hepatic injury after 30 minutes of ischemia during 70% partial hepatectomy
• impaired regenerative response after 70% hepatectomy
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nervous system
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• locomotor recovery from spinal cord injury occurs more rapidly than in controls
• slight improvement in tissue at 24 hours after injury but considerably improved relative to controls by 72 hours
• grossly normal at 7 days after injury compared to controls which show marked areas of necrosis with vacuolization of cells at day 7 and less pronounced necrosis at day 21
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skeleton
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• bone marrow cells incubated with 1,25(OH)2 vitamin D3 produce fewer osteoclasts than do cells from controls
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cellular
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• after 70% partial hepatectomy
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• impaired hepatocyte proliferation after 30 minutes of ischemia during 70% partial hepatectomy
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Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
| complement component 3 deficiency | DOID:8354 |
OMIM:613779 |
J:30152 | |
