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Malaria derived extracellular vesicles influence human neutrophils function
Author(s) -
Babatunde Kehinde Adebayo,
Walch Michael,
Fellay Isabelle,
KharoubiHess Solange,
Filgueira Luis,
Ghiran Ionita,
Mantel PierreYves
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.391.2
Subject(s) - innate immune system , immune system , biology , neutrophil extracellular traps , respiratory burst , malaria , immunology , microbiology and biotechnology , inflammation , plasmodium falciparum , secretion , population , medicine , biochemistry , environmental health
A dysfunctional innate immune response is believed to provide immune evasion of the malaria parasites, but also to cause increased susceptibility to bacterial infections. Neutrophils are the most abundant cells found in the blood circulation in direct contact with parasite infected red blood cells (iRBCs). However neutrophils population with reduced oxidative burst activities are present during malaria infection. These observations suggest that neutrophil responses are fundamentally defective in malaria patients. Extracellular vesicles (EVs) are iRBCs derived vesicles and contain both parasite and host materials, including microRNAs. In this present work we investigated, how EVs modulate neutrophil response. Results Interestingly, we have reported that malaria EVs contain miR451a, a miRNA that is known to regulate neutrophil activity. We have also monitored the uptake of EVs by neutrophils by fluorescence microscopy and real‐time polymerase chain reaction techniques. To address the role of miR451, we investigated the influence of malaria‐induced EVs on human neutrophil functions in vitro and the effect of miR451a on the transcriptional response in differentiated HL‐60 cells to bacterial infections. We demonstrated that EVs inhibit neutrophil function by inhibiting neutrophils ability to produce ROS and suppression of cytokine secretion. The neutrophils were also affected in their bactericidal activity. Conclusion Our data indicate that malaria EVs deliver miR‐451 into neutrophils to interfere with their capacity to kill bacteria. We describe a new mechanism of cellular communication between parasites and the host immune system. While EVs might increase tolerance to the parasites, they dramatically affect the resistance to a co‐infection by bacteria. The elucidation of the immune regulatory role of EVs might lead to the development of new diagnostic tools and therapies.