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2017 ; 129
(12
): 1669-1679
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Platelets activate a pathogenic response to blood-stage Plasmodium infection but
not a protective immune response
#MMPMID28096086
Gramaglia I
; Velez J
; Combes V
; Grau GE
; Wree M
; van der Heyde HC
Blood
2017[Mar]; 129
(12
): 1669-1679
PMID28096086
show ga
Clinical studies indicate that thrombocytopenia correlates with the development
of severe falciparum malaria, suggesting that platelets either contribute to
control of parasite replication, possibly as innate parasite killer cells or
function in eliciting pathogenesis. Removal of platelets by anti-CD41 mAb
treatment, platelet inhibition by aspirin, and adoptive transfer of wild-type
(WT) platelets to CD40-KO mice, which do not control parasite replication,
resulted in similar parasitemia compared with control mice. Human platelets at a
physiologic ratio of 1 platelet to 9 red blood cells (RBCs) did not inhibit the
in vitro development or replication of blood-stage Plasmodium falciparum The
percentage of Plasmodium-infected (iRBCs) with bound platelets during the
ascending parasitemia in Plasmodium chabaudi- and Plasmodium berghei-infected
mice and the 48-hour in vitro cycle of P falciparum was <10%. P chabaudi and P
berghei iRBCs with apoptotic parasites (TdT(+)) exhibited minimal platelet
binding (<5%), which was similar to nonapoptotic iRBCs. These findings
collectively indicate platelets do not kill bloodstage Plasmodium at
physiologically relevant effector-to-target ratios. P chabaudi primary and
secondary parasitemia was similar in mice depleted of platelets by mAb-injection
just before infection, indicating that activation of the protective immune
response does not require platelets. In contrast to the lack of an effect on
parasite replication, adoptive transfer of WT platelets to CD40-KO mice, which
are resistant to experimental cerebral malaria, partially restored experimental
cerebral malaria mortality and symptoms in CD40-KO recipients, indicating
platelets elicit pathogenesis and platelet CD40 is a key molecule.
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