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Updated: Nov 25, 2025
Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
BCG Provides Short-Term Protection from Experimental Cerebral Malaria in Mice
Julia Witschkowski1, Jochen Behrends2, Roland Frank3
1Junior Research Group Coinfection, Priority Area Infections, Research Center Borstel-Leibniz Lung Center, 23845 Borstel, Germany.
Abstract:
Clinical and experimental evidence suggests that the tuberculosis vaccine BCG offers protection against unrelated pathogens including the malaria parasite. Cerebral malaria (CM) is the most severe complication associated with Plasmodium falciparum infection in humans and is responsible for most of the fatalities attributed to malaria. We investigated whether BCG protected C57BL/6 mice from P. berghei ANKA (PbA)-induced experimental CM (ECM). The majority of PbA-infected mice that were immunized with BCG showed prolonged survival without developing clinical symptoms of ECM. However, this protective effect waned over time and was associated with the recovery of viable BCG from liver and spleen. Intriguingly, BCG-mediated protection from ECM was not associated with a reduction in parasite burden, indicating that BCG immunization did not improve anti-parasite effector mechanisms. Instead, we found a significant reduction in pro-inflammatory mediators and CD8+ T cells in brains of BCG-vaccinated mice. Together these data suggest that brain recruitment of immune cells involved in the pathogenesis of ECM decreased after BCG vaccination. Understanding the mechanisms underlying the protective effects of BCG on PbA-induced ECM can provide a rationale for developing effective adjunctive therapies to reduce the risk of death and brain damage in CM.
Insights
The tuberculosis vaccine BCG prolonged survival in mice with experimental cerebral malaria (ECM). BCG reduced brain inflammation and immune cell infiltration, but not parasite levels, suggesting a novel protective mechanism against severe malaria.
Area of Science:
- Immunology
- Infectious Diseases
- Vaccinology
Background:
- Cerebral malaria (CM) is a severe complication of Plasmodium falciparum infection, causing significant mortality.
- The Bacillus Calmette-Guérin (BCG) vaccine, primarily for tuberculosis, shows cross-protection against other pathogens.
- BCG's protective effects against malaria, particularly cerebral malaria, require further mechanistic investigation.
Purpose of the Study:
- To evaluate the efficacy of BCG vaccination against Plasmodium berghei ANKA (PbA)-induced experimental cerebral malaria (ECM) in C57BL/6 mice.
- To elucidate the immunological mechanisms underlying BCG-mediated protection in experimental cerebral malaria.
Main Methods:
- C57BL/6 mice were immunized with BCG prior to infection with PbA.
- Survival rates and clinical symptoms of ECM were monitored.
- Parasite burden, pro-inflammatory mediators, and CD8+ T cell infiltration in the brain were assessed.
Main Results:
- BCG vaccination significantly prolonged survival and reduced ECM development in PbA-infected mice.
- BCG-mediated protection waned over time and was associated with viable BCG in organs.
- Protection was not linked to reduced parasite burden but to decreased pro-inflammatory mediators and CD8+ T cells in the brain.
Conclusions:
- BCG vaccination confers partial protection against experimental cerebral malaria by modulating brain inflammation and immune cell infiltration.
- The findings suggest BCG's protective effect is independent of direct anti-parasite activity.
- Understanding these mechanisms could inform the development of adjunctive therapies for human cerebral malaria.
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