Plasmodium falciparum infection significantly impairs placental cytokine profile in HIV infected Cameroonian women.
BACKGROUND
Placental cytokines play crucial roles in the establishment and maintenance of pregnancy as well as protecting the foetus from infections. Previous studies have suggested the implication of infections such as P. falciparum and HIV in the stimulation of placental cytokines. This study assessed the impact of P. falciparum on placental cytokine profiles between HIV-1 positive and negative women.


METHODS
P. falciparum infection was checked in peripheral and placental blood of HIV-1 negative and positive women by the thick blood smear test. Cytokines proteins and messenger RNAs were quantified by ELISA and real time PCR, respectively. Non-parametric tests were used for statistical analyses.


RESULTS
Placental and peripheral P. falciparum infections were not significantly associated with HIV-1 infection (OR: 1.4; 95% confidence interval (95%CI): 0.5-4.2; p = 0.50 and OR: 0.6; 95%CI: 0.3-1.4; p = 0.26, respectively). Conversely, placental P. falciparum parasitemia was significantly higher in the HIV-1 positive group (p = 0.04). We observed an increase of TNF-alpha mRNA median levels (p = 0.02) and a trend towards a decrease of IL-10 mRNA (p = 0.07) in placenta from HIV-1 positive women compared to the HIV negative ones leading to a median TNF-alpha/IL-10 mRNA ratio significantly higher among HIV-1 positive than among HIV-1 negative placenta (p = 0.004; 1.5 and 0.8, respectively). Significant decrease in median secreted cytokine levels were observed in placenta from HIV-1 positive women as compared to the HIV negative however these results are somewhat indicative since it appears that differences in cytokine levels (protein or mRNA) between HIV-1 positive and negative women depend greatly on P.falciparum infection. Within the HIV-1 positive group, TNF-alpha was the only cytokine significantly associated with clinical parameters linked with HIV-1 MTCT such as premature rupture of membranes, CD4 T-cell number, plasma viral load and delay of NVP intake before delivery.


CONCLUSIONS
These results show that P. falciparum infection profoundly modifies the placenta cytokine environment and acts as a confounding factor, masking the impact of HIV-1 in co-infected women. This interplay between the two infections might have implications in the in utero MTCT of HIV-1 in areas where HIV-1 and P. falciparum co-circulate.
Kfutwah
Anfumbom
A
Virology Laboratory, Centre Pasteur du Cameroun, Yaoundé, Cameroon.
Mary
Jean Yves
JY
Lemen
Brigitte
B
Leke
Robert
R
Rousset
Dominique
D
Barré-Sinoussi
Françoise
F
Nerrienet
Eric
E
Menu
Elisabeth
E
Ayouba
Ahidjo
A
D000328:Adult; D002163:Cameroon; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005260:Female; D005786:Gene Expression Regulation; D015658:HIV Infections / Q000150:complications* / Q000378:metabolism* / Q000469:parasitology / Q000821:virology; D006679:HIV Seropositivity / Q000150:complications / Q000378:metabolism / Q000469:parasitology; D015497:HIV-1 / Q000502:physiology; D006801:Humans; D016778:Malaria, Falciparum / Q000150:complications* / Q000378:metabolism* / Q000469:parasitology / Q000821:virology; D018512:Parasitemia / Q000150:complications / Q000378:metabolism; D010920:Placenta / Q000378:metabolism* / Q000469:parasitology / Q000821:virology; D010963:Plasmodium falciparum / Q000502:physiology; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D013347:Subcellular Fractions / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism; D055815:Young Adult
D016207:Cytokines; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha