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

Yifat Ofir-Birin, Hila Ben Ami Pilo, Abel Cruz Camacho, Ariel Rudik, Anna Rivkin, Or-Yam Revach, Netta Nir, Tal Block Tamin, Paula Abou Karam, Edo Kiper, Yoav Peleg, Reinat Nevo, Aryeh Solomon, Tal Havkin-Solomon, Alicia Rojas, Ron Rotkopf, Ziv Porat, Dror Avni, Eli Schwartz, Thomas Zillinger, Gunther Hartmann, Antonella Pizio, Neils Ben Quashie, Rivka Dikstein, Motti Gerlic, Ana Claudia Torrecilhas, Carmit Levy, Esther N. M. Nolte-‘t Hoen, Andrew G. Bowie and Neta Regev-Rudzki ()
Additional contact information
Yifat Ofir-Birin: Weizmann Institute of Science
Hila Ben Ami Pilo: Weizmann Institute of Science
Abel Cruz Camacho: Weizmann Institute of Science
Ariel Rudik: Weizmann Institute of Science
Anna Rivkin: Weizmann Institute of Science
Or-Yam Revach: Weizmann Institute of Science
Netta Nir: Weizmann Institute of Science
Tal Block Tamin: Weizmann Institute of Science
Paula Abou Karam: Weizmann Institute of Science
Edo Kiper: Weizmann Institute of Science
Yoav Peleg: Weizmann Institute of Science
Reinat Nevo: Weizmann Institute of Science
Aryeh Solomon: Weizmann Institute of Science
Tal Havkin-Solomon: Weizmann Institute of Science
Alicia Rojas: Weizmann Institute of Science
Ron Rotkopf: Weizmann Institute of Science
Ziv Porat: Weizmann Institute of Science
Dror Avni: Sheba Medical Center
Eli Schwartz: Sheba Medical Center
Thomas Zillinger: University Hospital Bonn
Gunther Hartmann: University Hospital Bonn
Antonella Pizio: Technical University of Munich
Neils Ben Quashie: University of Ghana
Rivka Dikstein: Weizmann Institute of Science
Motti Gerlic: Tel Aviv University
Ana Claudia Torrecilhas: Federal University of São Paulo, UNIFESP
Carmit Levy: Tel Aviv University
Esther N. M. Nolte-‘t Hoen: Faculty of Veterinary Medicine, Utrecht University
Andrew G. Bowie: Trinity Biomedical Sciences Institute, Trinity College Dublin
Neta Regev-Rudzki: Weizmann Institute of Science

Nature Communications, 2021, vol. 12, issue 1, 1-15

Abstract: Abstract Pathogens are thought to use host molecular cues to control when to initiate life-cycle transitions, but these signals are mostly unknown, particularly for the parasitic disease malaria caused by Plasmodium falciparum. The chemokine CXCL10 is present at high levels in fatal cases of cerebral malaria patients, but is reduced in patients who survive and do not have complications. Here we show a Pf ‘decision-sensing-system’ controlled by CXCL10 concentration. High CXCL10 expression prompts P. falciparum to initiate a survival strategy via growth acceleration. Remarkably, P. falciparum inhibits CXCL10 synthesis in monocytes by disrupting the association of host ribosomes with CXCL10 transcripts. The underlying inhibition cascade involves RNA cargo delivery into monocytes that triggers RIG-I, which leads to HUR1 binding to an AU-rich domain of the CXCL10 3’UTR. These data indicate that when the parasite can no longer keep CXCL10 at low levels, it can exploit the chemokine as a cue to shift tactics and escape.

Date: 2021
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:12:y:2021:i:1:d:10.1038_s41467-021-24997-7

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DOI: 10.1038/s41467-021-24997-7

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