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Malaria parasites both repress host CXCL10 and use it as a cue for growth acceleration

Yifat Ofir-Birin1, Hila Ben Ami Pilo1, Abel Cruz Camacho1

  • 1Faculty of Biochemistry, Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, Israel.

Nature Communications
|August 12, 2021
PubMed

Insights

Malaria parasites use the host chemokine CXCL10 as a signal. High CXCL10 levels trigger parasite growth acceleration, while the parasite inhibits CXCL10 production to evade detection.

Area of Science:

  • Parasitology
  • Immunology
  • Molecular Biology

Background:

  • Pathogens utilize host molecular cues for life-cycle regulation, but these signals remain largely unidentified, especially in malaria.
  • The chemokine CXCL10 is elevated in fatal cerebral malaria and reduced in survivors without complications.

Purpose of the Study:

  • To investigate the role of CXCL10 in Plasmodium falciparum pathogenesis and host-parasite interactions.
  • To elucidate the molecular mechanisms by which P. falciparum senses and responds to CXCL10 concentrations.

Main Methods:

  • Analysis of CXCL10 levels in malaria patients.
  • Investigating P. falciparum's response to varying CXCL10 concentrations.
  • Studying the inhibition of CXCL10 synthesis by P. falciparum in monocytes.
  • Elucidating the molecular cascade involving RNA cargo, RIG-I, and HUR1.

Main Results:

  • P. falciparum possesses a "decision-sensing-system" regulated by CXCL10 concentration.
  • High CXCL10 induces P. falciparum to accelerate growth as a survival strategy.
  • P. falciparum actively inhibits host CXCL10 synthesis by disrupting ribosome-transcript association in monocytes.
  • The inhibition involves RNA cargo delivery, RIG-I activation, and HUR1 binding to the CXCL10 3'UTR.

Conclusions:

  • CXCL10 acts as a critical host cue influencing P. falciparum behavior.
  • P. falciparum manipulates host immune responses by inhibiting CXCL10 production.
  • This parasite-host interaction highlights a novel mechanism for pathogen survival and immune evasion in malaria.

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