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Updated: Jul 25, 2026
Isolation and Analysis of Brain-sequestered Leukocytes from Plasmodium berghei ANKA-infected Mice
Published on: January 2, 2013
IL35 modulation altered survival, cytokine environment and histopathological consequences during malaria infection in
Ramatu Omenesa Bello1,2, Maizaton Atmadini Abdullah3, Roslaini Abd Majid4
1Department of Human Anatomy, Faculty of Medicine and Health Sciences, University Putra Malaysia, 43400, Serdang, Selangor, Malaysia.
Background:
The immune modulating potential of IL-35 in multiple human disorders has been reported. Consequent upon the recognition of inflammatory cytokine activation and its preponderance for mediating pathology during malaria infection, the study aimed to characterize the expression and functional contribution(s) of IL-35 in Plasmodium berghei (strain ANKA) infected mice.
Methods:
Plasmodium berghei infection in male ICR mice was used as the rodent model of choice. The time course of IL-35 expression in the systemic circulation and tissues of P. berghei infected mice as well as their healthy control counterparts was assessed by enzyme linked immunosorbent assay and immunohistochemistry respectively. The effect of modulating IL-35 by recombinant IL-35 protein or neutralizing anti-Epstein-Barr virus-induced gene 3 antibody on the cytokine environment during P. berghei infection was assessed by flow cytometry. Furthermore, the influence of modulating IL-35 on histopathological hallmarks of malaria and disease progression was evaluated.
Results:
Interleukin-35 was significantly up regulated in serum and tissues of P. berghei infected mice and correlated with parasitaemia. Neutralization of IL-35 significantly enhanced the release of IFN-γ, decreased the expression of IL-6 and decreased parasitaemia patency. Neutralization of IL-35 was also associated with a tendency towards increased survival as well as the absence of pathological features associated with malaria infection unlike recombinant IL-35 protein administration which sustained a normal course of infection and unfavourable malaria associated histological outcomes in P. berghei infected mice.
Conclusion:
These results indicate the involvement of IL-35 in P. berghei induced malaria infection. IL-35 neutralization strategies may represent viable therapeutic modalities beneficial for the resolution of malaria infection.
Insights
Interleukin-35 (IL-35) is upregulated during Plasmodium berghei malaria infection. Neutralizing IL-35 in mice reduced parasite levels and improved survival, suggesting IL-35 as a therapeutic target for malaria.
Area of Science:
- Immunology
- Infectious Diseases
- Parasitology
Background:
- Interleukin-35 (IL-35) is known for immune modulation in various disorders.
- Inflammatory cytokines, including IL-35, play a role in malaria pathology.
- Understanding IL-35's role in Plasmodium berghei infection is crucial.
Purpose of the Study:
- To characterize IL-35 expression during Plasmodium berghei infection in mice.
- To investigate the functional role of IL-35 in malaria pathogenesis.
- To evaluate IL-35 as a potential therapeutic target.
Main Methods:
- Rodent model: Plasmodium berghei infected ICR mice.
- Assessed IL-35 expression via ELISA and immunohistochemistry.
- Modulated IL-35 using recombinant protein or neutralizing antibodies, analyzed cytokine profiles (flow cytometry), histopathology, and disease progression.
Main Results:
- IL-35 was significantly upregulated in infected mice, correlating with parasitemia.
- IL-35 neutralization enhanced IFN-γ, reduced IL-6, decreased parasitemia, and improved survival.
- Recombinant IL-35 sustained infection and associated pathology.
Conclusions:
- IL-35 is involved in Plasmodium berghei malaria pathogenesis.
- IL-35 neutralization presents a potential therapeutic strategy for malaria resolution.
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