title: Plasmodium falciparum exposure in utero, maternal age and parity influence the innate activation of foetal antigen presenting cells.
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.
  
  
  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.
  
  
  CONCLUSIONS
  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.
  
  
  CONCLUSIONS
  These data advocate a possible mechanism by which PAM may modulate foetal/neonatal innate immunity.
authors.affiliation: UR010, Mother and Child Health in the Tropics, Institut de Recherche pour le Développement (IRD), Cotonou, Benin.
authors.forename: Nadine
authors.initials: N
authors.lastname: Fievet
authors.forename: Stefania
authors.initials: S
authors.lastname: Varani
authors.forename: Samad
authors.initials: S
authors.lastname: Ibitokou
authors.forename: Valérie
authors.initials: V
authors.lastname: Briand
authors.forename: Stéphanie
authors.initials: S
authors.lastname: Louis
authors.forename: René Xavier
authors.initials: RX
authors.lastname: Perrin
authors.forename: Achille
authors.initials: A
authors.lastname: Massougbogji
authors.forename: Anne
authors.initials: A
authors.lastname: Hosmalin
authors.forename: Marita
authors.initials: M
authors.lastname: Troye-Blomberg
authors.forename: Philippe
authors.initials: P
authors.lastname: Deloron
mesh_terms: D000328:Adult; D000938:Antigen-Presenting Cells / Q000276:immunology; D000953:Antigens, Protozoan / Q000276:immunology; D001541:Benin; D016207:Cytokines / Q000097:blood* / Q000276:immunology; D003713:Dendritic Cells / Q000276:immunology; D005260:Female; D005312:Fetal Blood / Q000166:cytology / Q000276:immunology* / Q000469:parasitology; D005434:Flow Cytometry; D006801:Humans; D007113:Immunity, Innate / Q000276:immunology; D018445:Infectious Disease Transmission, Vertical; D008213:Lymphocyte Activation / Q000502:physiology*; D016778:Malaria, Falciparum / Q000276:immunology / Q000635:transmission*; D008423:Maternal Age; D010298:Parity; D010963:Plasmodium falciparum / Q000276:immunology / Q000302:isolation & purification*; D011247:Pregnancy; D015597:Pregnancy Complications, Parasitic / Q000276:immunology; D051193:Toll-Like Receptors / Q000502:physiology; D014599:Uterus / Q000276:immunology / Q000469:parasitology; D055815:Young Adult
chemical_list: D000953:Antigens, Protozoan; D016207:Cytokines; D051193:Toll-Like Receptors