Analysis Tools
mortality/aging
|
• Background Sensitivity: about 40% of mice die within 10 days of infection with the P. berghei parasite compared to less than 15% lethality for BALB/c mice and 100% lethality for C57BL/6 mice
|
immune system
|
• total and parasite specific IgG levels are significantly less thanin BALB/c controls starting one week after infection with P. berghei
|
|
• parasite specific IgG1 levels are significantly less than BALB/c controls starting one week after infection with P. berghei
|
|
• parasite specific levels are significantly less than BALB/c controls between 3 and 10 days after infection with P. berghei
|
|
• parasite specific levelsof IgG2b are significantly less than in BALB/c controls starting one week after infection with P. berghei with 8-fold differences occurring two weeks after infection
|
|
• parasite specific IgG3 levels are significantly less than BALB/c controls starting 10 days after infection with P. berghei
|
|
• both parasite specific and total levels of IgM remain elevated 8-14 days after infection with P. berghei while IgM levels decrease in BALB/c controls
|
|
• circulating IFN-gamma levels are significantly higher 3, 5, and 7 days after P. berghei infection compared to BALB/c control mice
|
|
• splenocytes from malaria-infected mice produce much less IL-4 upon encounter with parasite antigens compared to BALB/c controls
|
|
• Background Sensitivity: about 40% of mice die within 10 days of infection with the P. berghei parasite compared to less than 15% lethality for BALB/c mice and 100% lethality for C57BL/6 mice
|
|
• mice have more severe vascular occlusion in the brain caused by parasitized erythrocytes and macrophages than in control BALB/c mice seven days after infection
• pulmonary edema is more severe 7-10 days after P. berghei infection than in BALB/c control
• hemoglobin levels drop at a faster rate than in BALB/c controls after infection with P. berghei, reaching a level that is 20% of normal two weeks after infection
|
|
• Background Sensitivity: mice have low titers of murine cytomegalovirus (CMV) in their spleens 2 to 6 days after infection compared to control BALB/c mice that have 1000-fold higher titers
(J:22486)
• Background Sensitivity: this resistance is mediated by natural killer (NK) cells as demonstrated by a lack of resistance to CMV when NK cells are depleted by antibody treatment
(J:22486)
• Background Sensitivity: mice have a 1000-fold lower viral titer in the spleen three days after CMV infection compared to BALB/c controls
(J:79093)
• Background Sensitivity: this resistance to CMV infection is similar to what is observed in C57BL/6 mice
(J:79093)
|
homeostasis/metabolism
|
• circulating IFN-gamma levels are significantly higher 3, 5, and 7 days after P. berghei infection compared to BALB/c control mice
|
|
• TGF-beta levels are slightly lower than BALB/c controls two weeks after P. berghei infection
|
hematopoietic system
|
• total and parasite specific IgG levels are significantly less thanin BALB/c controls starting one week after infection with P. berghei
|
|
• parasite specific IgG1 levels are significantly less than BALB/c controls starting one week after infection with P. berghei
|
|
• parasite specific levels are significantly less than BALB/c controls between 3 and 10 days after infection with P. berghei
|
|
• parasite specific levelsof IgG2b are significantly less than in BALB/c controls starting one week after infection with P. berghei with 8-fold differences occurring two weeks after infection
|
|
• parasite specific IgG3 levels are significantly less than BALB/c controls starting 10 days after infection with P. berghei
|
|
• both parasite specific and total levels of IgM remain elevated 8-14 days after infection with P. berghei while IgM levels decrease in BALB/c controls
|
