Analysis Tools
mortality/aging
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• increased mortality from GBS infection compared to controls is limited to the first 3 days after challenge
• mice challenged with group B Streptococci (GBS) infection become bacteremic within 3 days and die or clear bacteria and survive; C4b-deficient mice challenged with GBS infection showed a decreased LD50 dose compared to immunocompetent controls (LD50 dose: control 6.3 x 104 vs. 2.4 x 103 in C4b-deficient mice)
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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)
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immune system
| N |
• secondary immune responses are similar in wild-type and mutant mice, so helper T cell function is normal
(J:64282)
• B cells from deficient mice show normal proliferative effects in response to surface IgM crosslinking
(J:64282)
• serum from C4-deficient mice has similar antibody-mediated opsonophagocytic killing of GBS to control serum
(J:30152)
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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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• 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
• in response to immunization with bacteriophage (phiX174), a T cell dependent antigen, C4b-deficient mice mount a weak Ig M response but fail to switch to IgG
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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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• when pregnant dams are immunized with immune rabbit serum, pups are protected against lethal challenge on day 2 of life because of transfer of maternal antibodies to the pups (15/16 pups survive, similar to controls)
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• increased mortality from GBS infection compared to controls is limited to the first 3 days after challenge
• mice challenged with group B Streptococci (GBS) infection become bacteremic within 3 days and die or clear bacteria and survive; C4b-deficient mice challenged with GBS infection showed a decreased LD50 dose compared to immunocompetent controls (LD50 dose: control 6.3 x 104 vs. 2.4 x 103 in C4b-deficient mice)
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homeostasis/metabolism
| N |
• response to renal ischemia reperfusion injury is the same as in wild-type mice
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hematopoietic system
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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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cardiovascular system
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• upeon reperfusion of ischemic intestine (jejunum), permeability index (PI) of injured C4b-deficient mice is reduced compared to control treated wild-type (PI of 2.20 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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liver/biliary system
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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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