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Interaction between Plasmodium Glycosylphosphatidylinositol and the Host Protein Moesin Has No Implication in Malaria

Josefine Dunst1,2, Nahid Azzouz1,3, Xinyu Liu4

  • 1Institute of Chemistry and Biochemistry, Free University BerlinBerlin, Germany.

Frontiers in Cellular and Infection Microbiology
|June 1, 2017
PubMed

Insights

This study investigated the role of the host protein moesin in severe malaria pathology. While Plasmodium falciparum GPI and moesin interact in vitro, moesin is not essential for malaria-induced inflammation or cerebral pathology.

Area of Science:

  • Immunology
  • Parasitology
  • Molecular Biology

Background:

  • Severe malaria pathology is linked to the Plasmodium falciparum glycosylphosphatidylinositol (GPI) anchor, which stimulates pro-inflammatory responses.
  • Toll-like receptors (TLRs) 2 and 4 are implicated in GPI-induced immunity, but are dispensable for severe malaria.
  • Alternative GPI receptors are sought to explain malaria pathogenesis.

Purpose of the Study:

  • To identify alternative host receptors for Plasmodium falciparum GPI.
  • To investigate the physiological relevance of moesin-GPI interaction in malaria pathology.

Main Methods:

  • In vitro interaction assays between Plasmodium GPI and host proteins.
  • In vitro and in vivo experiments to assess moesin's role in malaria.
  • Analysis of pro-inflammatory immune responses and cerebral pathology in malaria models.

Main Results:

  • The host protein moesin was identified as an in vitro interaction partner of Plasmodium GPI.
  • Despite in vitro interaction, moesin did not critically mediate Plasmodium-induced pro-inflammatory responses.
  • Moesin was found to be dispensable for malaria-associated cerebral pathology.

Conclusions:

  • Moesin is not a critical host receptor mediating Plasmodium GPI-induced inflammation or severe malaria pathology.
  • The findings suggest alternative pathways or receptors are involved in GPI-mediated severe malaria.
  • Further research is needed to elucidate the precise mechanisms of GPI-induced severe malaria.
Keywords:
ERMGPIPlasmodiumcerebral malariamoesin

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