Lack of an association between antibodies to Plasmodium falciparum glycosylpliosphatidylinositols and malaria-associated placental changes in Cameroonian women with preterm and full-term deliveries

Amorsolo L. Suguitan, Channe Gowda, Genevieve Fouda, Lucy Thuita, Ainong Zhou, Rosine Djokam, Simon Metenou, Rose G.F. Leke, Diane Wallace Taylor

Research output: Contribution to journalArticle

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Abstract

Sequestration of Plasmodium falciparum parasites within the placenta often leads to an accumulation of macrophages within the intervillous space and increased production of tumor necrosis factor alpha (TNF-α), a cytokine associated with placental pathology and poor pregnancy outcomes. P. falciparum glycosylphosphatidylinositol (GPI) anchors have been shown to be the major parasite component that induces TNF-7alpha; production by monocytes and macrophages. Antibodies against P. falciparum GPI (anti-PfGPI), however, can inhibit the induction of TNF-α and inflammation. Thus, the study was undertaken to determine whether anti-PfGPI antibodies down-regulate inflammatory-type changes in the placentas of women with malaria. Anti-PfGPI immunoglobtitin M (IgM) and IgG levels were measured in 380 pregnant women with or without placental malaria, including those who delivered prematurely and at term. Results showed that anti-PfGPI antibody levels increased with gravidity and age and that malaria infection boosted anti-PfGPI antibodies in pregnant women. However, no association was found between anti-PfGPI antibodies and placental TNF-α levels or the presence of acute or chronic placental malaria. Furthermore, anti-PfGPI antibody levels were similar in women with preterm and full-term deliveries and were not associated with an increase in infant birth weight. Thus, these results fail to support a strong role for anti-PfGPI antibodies in the prevention of chronic placental malaria infections and malaria-associated poor birth outcomes.

Original languageEnglish (US)
Pages (from-to)5267-5273
Number of pages7
JournalInfection and Immunity
Volume72
Issue number9
DOIs
StatePublished - Sep 1 2004

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Falciparum Malaria
Plasmodium falciparum
Antibodies
Malaria
Tumor Necrosis Factor-alpha
Glycosylphosphatidylinositols
Placenta
Pregnant Women
Parasites
Macrophages
Gravidity
Pregnancy Outcome
Infection
Birth Weight
Monocytes
Down-Regulation
Immunoglobulin G

All Science Journal Classification (ASJC) codes

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Cite this

Suguitan, Amorsolo L. ; Gowda, Channe ; Fouda, Genevieve ; Thuita, Lucy ; Zhou, Ainong ; Djokam, Rosine ; Metenou, Simon ; Leke, Rose G.F. ; Taylor, Diane Wallace. / Lack of an association between antibodies to Plasmodium falciparum glycosylpliosphatidylinositols and malaria-associated placental changes in Cameroonian women with preterm and full-term deliveries. In: Infection and Immunity. 2004 ; Vol. 72, No. 9. pp. 5267-5273.
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abstract = "Sequestration of Plasmodium falciparum parasites within the placenta often leads to an accumulation of macrophages within the intervillous space and increased production of tumor necrosis factor alpha (TNF-α), a cytokine associated with placental pathology and poor pregnancy outcomes. P. falciparum glycosylphosphatidylinositol (GPI) anchors have been shown to be the major parasite component that induces TNF-7alpha; production by monocytes and macrophages. Antibodies against P. falciparum GPI (anti-PfGPI), however, can inhibit the induction of TNF-α and inflammation. Thus, the study was undertaken to determine whether anti-PfGPI antibodies down-regulate inflammatory-type changes in the placentas of women with malaria. Anti-PfGPI immunoglobtitin M (IgM) and IgG levels were measured in 380 pregnant women with or without placental malaria, including those who delivered prematurely and at term. Results showed that anti-PfGPI antibody levels increased with gravidity and age and that malaria infection boosted anti-PfGPI antibodies in pregnant women. However, no association was found between anti-PfGPI antibodies and placental TNF-α levels or the presence of acute or chronic placental malaria. Furthermore, anti-PfGPI antibody levels were similar in women with preterm and full-term deliveries and were not associated with an increase in infant birth weight. Thus, these results fail to support a strong role for anti-PfGPI antibodies in the prevention of chronic placental malaria infections and malaria-associated poor birth outcomes.",
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Lack of an association between antibodies to Plasmodium falciparum glycosylpliosphatidylinositols and malaria-associated placental changes in Cameroonian women with preterm and full-term deliveries. / Suguitan, Amorsolo L.; Gowda, Channe; Fouda, Genevieve; Thuita, Lucy; Zhou, Ainong; Djokam, Rosine; Metenou, Simon; Leke, Rose G.F.; Taylor, Diane Wallace.

In: Infection and Immunity, Vol. 72, No. 9, 01.09.2004, p. 5267-5273.

Research output: Contribution to journalArticle

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AU - Suguitan, Amorsolo L.

AU - Gowda, Channe

AU - Fouda, Genevieve

AU - Thuita, Lucy

AU - Zhou, Ainong

AU - Djokam, Rosine

AU - Metenou, Simon

AU - Leke, Rose G.F.

AU - Taylor, Diane Wallace

PY - 2004/9/1

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N2 - Sequestration of Plasmodium falciparum parasites within the placenta often leads to an accumulation of macrophages within the intervillous space and increased production of tumor necrosis factor alpha (TNF-α), a cytokine associated with placental pathology and poor pregnancy outcomes. P. falciparum glycosylphosphatidylinositol (GPI) anchors have been shown to be the major parasite component that induces TNF-7alpha; production by monocytes and macrophages. Antibodies against P. falciparum GPI (anti-PfGPI), however, can inhibit the induction of TNF-α and inflammation. Thus, the study was undertaken to determine whether anti-PfGPI antibodies down-regulate inflammatory-type changes in the placentas of women with malaria. Anti-PfGPI immunoglobtitin M (IgM) and IgG levels were measured in 380 pregnant women with or without placental malaria, including those who delivered prematurely and at term. Results showed that anti-PfGPI antibody levels increased with gravidity and age and that malaria infection boosted anti-PfGPI antibodies in pregnant women. However, no association was found between anti-PfGPI antibodies and placental TNF-α levels or the presence of acute or chronic placental malaria. Furthermore, anti-PfGPI antibody levels were similar in women with preterm and full-term deliveries and were not associated with an increase in infant birth weight. Thus, these results fail to support a strong role for anti-PfGPI antibodies in the prevention of chronic placental malaria infections and malaria-associated poor birth outcomes.

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