<i>Plasmodium falciparum</i>Induces a Th1/Th2 Disequilibrium, Favoring the Th1‐Type Pathway, in the Human Placenta

Fiévet, Nadine; Moussa, Marlène; Tami, Germaine; Maubert, Bertrand; Cot, Michel; Deloron, Philippe; Chaouat, G.

doi:10.1086/320201

Cited by 94 publications

(88 citation statements)

References 12 publications

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“…Our data confirm that the placenta is the likely site for production of TNF-␣. Similar findings have been reported for women from Kenya and Cameroon (8,9). In each case, levels of TNF-␣ were higher than those we detected, and serum (not plasma) was used for measurements.…”

Section: Discussionsupporting

confidence: 89%

“…In placental malaria infection, a proinflammatory or Th1 cytokine response appears common. Cytokines associated with placental malaria have been measured by a number of techniques, including assays of placental serum (8,9), RNase protection assay (18), and secretion in vitro by placental blood cells, purified mononuclear cells, or villous explants (5,8,16,17). Malaria-associated increases in tumor necrosis factor alpha (TNF-␣), interleukin 8 (IL-8), gamma interferon (IFN-␥), IL-6, and IL-10 have been reported in one or more assay systems, but only increased placental TNF-␣ levels have been repeatedly associated with LBW (9,18).…”

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confidence: 99%

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Placental Tumor Necrosis Factor Alpha but Not Gamma Interferon Is Associated with Placental Malaria and Low Birth Weight in Malawian Women

et al. 2003

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Malaria in pregnancy predisposes to maternal anemia and low birth weight (LBW). We examined the possible roles of the cytokines tumor necrosis factor alpha (TNF-␣) and gamma interferon (IFN-␥) in these adverse outcomes. We measured cytokine concentrations in placental, peripheral, and cord blood plasma in relation to malaria parasitemia and placental monocyte accumulation in 276 Malawian women. Maternal hemoglobin concentration, human immunodeficiency virus status, and infant birth weight were determined. Concentrations of TNF-␣ in placental blood were correlated with densities of Plasmodium falciparum-infected erythrocytes (P < 0.0001) and of intervillous monocyte infiltrates (P < 0.0001) on placental histology. Peripheral blood TNF-␣ concentrations were relatively low and were weakly associated with malaria. TNF-␣ concentrations were higher in placental blood, where they were strongly associated with malaria. Placental plasma TNF-␣ levels were higher in women who had LBW babies (P ‫؍‬ 0.0027), women with febrile symptoms (P < 0.0001), and teenage mothers (P ‫؍‬ 0.04) than in other women. The presence of TNF-␣ in cord blood was not associated with malaria infection. IFN-␥ levels were infrequently elevated, and elevated IFN-␥ levels were not associated with poor pregnancy outcomes. Placental production of TNF-␣, but not of IFN-␥, may be implicated in impaired fetal growth in Malawian women.

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Section: Discussionsupporting

confidence: 89%

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confidence: 99%

Placental Tumor Necrosis Factor Alpha but Not Gamma Interferon Is Associated with Placental Malaria and Low Birth Weight in Malawian Women

et al. 2003

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“…Our study adds Salmonella to the list of pathogens such as Toxoplasma, Chlamydia, Listeria, and Plasmodium that preferentially invade the placenta and may cause abortion through local inflammation (15,16,31,32). The placental interface does express TLRs and can trigger the innate cascade (32,33) to protect the host.…”

Section: Discussionmentioning

confidence: 99%

Pregnancy Impairs the Innate Immune Resistance toSalmonella typhimuriumLeading to Rapid Fatal Infection

Pejčić-Karapetrović

Gurnani

Russell

et al. 2007

The Journal of Immunology

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Typhoid fever and gastroenteritis caused by Salmonella enterica species are increasing globally. Pregnancy poses a high risk, but it is unclear how maternal immunity to infection is altered. In mice, susceptible strains die of S. enterica serovar typhimurium (ST) infection within 7 days whereas resistant mice (129×1/SvJ) develop a chronic infection. We found that virulent ST infection during pregnancy, in normally resistant 129×1/SvJ mice, evoked ∼100% fetal loss and surprisingly >60% host fatality, with a median survival of 6 days. Splenic bacterial load was 1000-fold higher in pregnant mice. This correlated to a diminished splenic recruitment/expansion of innate immune cells: dendritic cells, neutrophils, and NK cells. In particular, the splenic expansion and activation of NK cells postinfection seen in nonpregnant mice was lacking in pregnancy. Most notably, pregnant-infected mice had decreased production of serum IL-12 and increased IL-6 levels. Moreover, uteroplacental tissue of pregnant-infected mice exhibited an ∼40-fold increase in IL-6 mRNA expression relative to noninfected placenta, whereas IL-12p40 was not increased. In vivo blocking of IL-6 significantly reduced the splenic bacterial burden in pregnant mice yet failed to prevent fetal loss. Fetal demise correlated to the rapidity of infection; by 14 h, ST expanded to >105 in the placenta and had reached the fetus. Therefore, the preferential placental expansion of ST plausibly altered the inflammatory response toward IL-6 and away from IL-12, reducing the recruitment/activation of splenic innate immune cells. Thus, highly virulent pathogens may use placental invasion to alter systemic host resistance to infection.

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“…Albeit the immense importance of cell derived factors in the immune response against Plasmodium spp., their overproduction might pose a risk for the success of the pregnancy. Since both placental and fetal cells exposed to antigens can be the source of pro-inflammatory cytokines, they may jeopardize full pregnancy completion [96,97].…”

Section: Specific Antimalarial Immunity During Pregnancymentioning

confidence: 99%

Immune responses during gestational malaria: a review of the current knowledge and future trend of research

Maestre

Carmona‐Fonseca

2014

J Infect Dev Ctries

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Women pregnant with their first child are susceptible to severe P. falciparum disease from placental malaria because they lack immunity to placenta-specific cytoadherence proteins. In subsequent pregnancies, as immunity against placental parasites is acquired, there is a reduced risk of adverse effects of malaria on the mother and fetus and asymptomatic parasitaemia is common. In the case of vivax malaria, with increasing reports of severe cases in Asia and South America, the effects of infection by this species during pregnancy remain to be elucidated. This review summarized the main aspects involved in the acquisition of specific antimalarial immune responses during pregnancy with emphasis in research carried out in America and Asia, in order to offer a framework of interpretation for studies on pregnant women with malaria which are recently being produced in these regions. The authors conclude that (1) Effective humoral responses during gestational malaria are mainly directed against variant surface antigens codified by genes of the var2Csa family of P. falciparum; (2) Acquisition of immunity against these variant antigens depends on the degree and intensity of transmission, and the chance increases with age and successive pregnancies; (3) Antibody development is guided by specific cellular immune responses in cases of placental and maternal infection, and (4) The study of the significance of acquisition of specific immunity against both P. falciparum and P. vivax in America, should be performed.

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Plasmodium falciparumInduces a Th1/Th2 Disequilibrium, Favoring the Th1‐Type Pathway, in the Human Placenta

Cited by 94 publications

References 12 publications

Placental Tumor Necrosis Factor Alpha but Not Gamma Interferon Is Associated with Placental Malaria and Low Birth Weight in Malawian Women

Placental Tumor Necrosis Factor Alpha but Not Gamma Interferon Is Associated with Placental Malaria and Low Birth Weight in Malawian Women

Pregnancy Impairs the Innate Immune Resistance toSalmonella typhimuriumLeading to Rapid Fatal Infection

Immune responses during gestational malaria: a review of the current knowledge and future trend of research

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