Research

Plasmodium falciparum exposure in utero, maternal age and parity influence the innate activation of foetal antigen presenting cells

Nadine Fievet^1,2* , Stefania Varani^3,4* , Samad Ibitokou¹ , Valérie Briand² , Stéphanie Louis⁶ , René Xavier Perrin⁵ , Achille Massougbogji⁵ , Anne Hosmalin^6,7 , Marita Troye-Blomberg³ and Philippe Deloron²

¹  UR010, Mother and Child Health in the Tropics, Institut de Recherche pour le Développement (IRD), Cotonou, Benin

²  UR010, IRD, IFR 71 Université René Descartes, 75006 Paris, France

³  Department of Immunology, Wenner-Gren Institute, Stockholm University, Stockholm, Sweden

⁴  Department of Hematology and Oncology, "L. and A. Seragnoli" University of Bologna, Bologna, Italy

⁵  Faculté des Science de la Santé, Cotonou, Benin

⁶  Institut Cochin, Université Paris Descartes, CNRS (UMR 8104), Paris, France

⁷  Inserm, U567, Paris, France

author email corresponding author email* Contributed equally

Malaria Journal 2009, 8:251doi:10.1186/1475-2875-8-251

Published:	5 November 2009

Abstract

Background

Malaria in pregnancy is associated with immunological abnormalities in the newborns, such as hampered T-helper 1 responses and increased T-regulatory responses, while the effect of maternal Plasmodium falciparum infection on foetal innate immunity is still controversial.

Materials and methods

The immunophenotype and cytokine release by dendritic cells (DC) and monocytes were evaluated in cord blood from 59 Beninese women with or without malaria infection by using flow cytometry.

Results

Accumulation of malaria pigment in placenta was associated with a partial maturation of cord blood myeloid and plasmacytoid DC, as reflected by an up-regulated expression of the major histocompatibility complex class II molecules, but not CD86 molecules. Cells of newborns of mothers with malaria pigment in their placenta also exhibited significantly increased cytokine responses upon TLR9 stimulation. In addition, maternal age and parity influenced the absolute numbers and activation status of cord blood antigen-presenting cells. Lastly, maternal age, but not parity, influenced TLR3, 4 and 9 responses in cord blood cells.

Discussion

Our findings support the view that placental parasitization, as indicated by the presence of malaria pigment in placental leukocytes, is significantly associated with partial maturation of different DC subsets and also to slightly increased responses to TLR9 ligand in cord blood. Additionally, other factors, such as maternal age and parity should be taken into consideration when analysing foetal/neonatal innate immune responses.

Conclusion

These data advocate a possible mechanism by which PAM may modulate foetal/neonatal innate immunity.