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Neutrophil alterations in pregnancy‐associated malaria and induction of neutrophil chemotaxis by Plasmodium falciparum
Author(s) -
Boström S.,
Schmiegelow C.,
Abu Abed U.,
Minja D. T. R.,
Lusingu J.,
Brinkmann V.,
Honkpehedji Y. J.,
Loembe M. M.,
Adegnika A. A.,
Mordmüller B.,
TroyeBlomberg M.,
Amulic B.
Publication year - 2017
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12433
Subject(s) - immunology , plasmodium falciparum , biology , placenta , malaria , monocyte , context (archaeology) , chemotaxis , pathogenesis , immune system , pregnancy , fetus , receptor , paleontology , biochemistry , genetics
Summary Pregnancy‐associated malaria ( PAM ) is a severe form of the disease caused by sequestration of Plasmodium falciparum ‐infected red blood cells ( iRBC s) in the developing placenta. Pathogenesis of PAM is partially based on immunopathology, with frequent monocyte infiltration into the placenta. Neutrophils are abundant blood cells that are essential for immune defence but may also cause inflammatory pathology. Their role in PAM remains unclear. We analysed neutrophil alterations in the context of PAM to better understand their contribution to disease development. Pregnant women exposed to Plasmodium falciparum had decreased numbers of circulating neutrophils. Placental‐like BeWo cells stimulated with malaria parasites produced the neutrophil chemoattractant IL ‐8 and recruited neutrophils in a trans‐well assay. Finally, immunostaining of a PAM placenta confirmed neutrophil accumulation in the intervillous space. Our data indicate neutrophils may play a role in placental malaria and should be more closely examined as an etiological agent in the pathophysiology of disease.