Nrf2 and CD36 in Malaria: A New Pathway for Treatment
Author Information
Author(s): Olagnier David, Lavergne Rose-Anne, Meunier Etienne, Lefèvre Lise, Dardenne Christophe, Aubouy Agnès, Benoit-Vical Françoise, Ryffel Bernhard, Coste Agnès, Berry Antoine, Pipy Bernard
Primary Institution: Université de Toulouse
Hypothesis
Nrf2 may substitute PPARγ to promote CD36 expression and enhance Plasmodium clearance during inflammatory processes.
Conclusion
Nrf2 activators improve CD36 expression and enhance the clearance of malaria parasites in inflammatory conditions.
Supporting Evidence
- Nrf2 activators enhance CD36 expression in both murine and human macrophages.
- Inflammatory conditions downregulate CD36 expression, worsening malaria infection.
- Nrf2 can promote CD36 expression independently of PPARγ.
- SFN treatment improves survival rates in a murine model of severe malaria.
- CD36 is crucial for the phagocytosis of Plasmodium falciparum by macrophages.
Takeaway
This study shows that a protein called Nrf2 can help our immune cells better fight malaria by increasing a receptor called CD36, especially when there is inflammation.
Methodology
The study involved in vitro experiments on murine and human macrophages and in vivo experiments using a murine model of severe malaria.
Limitations
The study primarily focuses on murine models, which may not fully replicate human responses.
Statistical Information
P-Value
p<0.01
Statistical Significance
p<0.01
Digital Object Identifier (DOI)
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