ArticlePloS one2009
C5a enhances dysregulated inflammatory and angiogenic responses to malaria in vitro: potential implications for placental malaria.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 78 citations in OpenAlex.
- Impact of Malaria Infection on the Diagnostic Performance of Adipsin for Preeclampsia in Pregnancy: A Case-Control Study.Journal of pregnancy · 2026Article
- Complement System Activation Is a Plasma Biomarker Signature during Malaria in Pregnancy.Genes · 2023Article
- Effect of porcine reproductive and respiratory syndrome virus 2 on angiogenesis and cell proliferation at the maternal-fetal interface.Veterinary pathology · 2022Article
- HIF-1α regulated pathomechanism of low birth weight through angiogenesis factors in placentalF1000Research · 2022Article
- Placental Immune Responses to Viruses: Molecular and Histo-Pathologic Perspectives.International journal of molecular sciences · 2021Review
- Malaria in Pregnancy: From Placental Infection to Its Abnormal Development and Damage.Frontiers in microbiology · 2021Review
- Beyond Binding: The Outcomes of Antibody-Dependent Complement Activation in Human Malaria.Frontiers in immunology · 2021Review
- Circulating Cytokines Associated with Poor Pregnancy Outcomes in Beninese Exposed to Infection with Plasmodium falciparum.Infection and immunity · 2020Article
- Association of Angiopoietin Dysregulation in Placental Malaria with Adverse Birth Outcomes.Disease markers · 2020Article
- New insights into microvascular injury to inform enhanced diagnostics and therapeutics for severe malaria.Virulence · 2019Review
- Anti-PCSK9 antibodies inhibit pro-atherogenic mechanisms in APOE*3Leiden.CETP mice.Scientific reports · 2019Article
- Significance of Complement System in Ischemic Stroke: A Comprehensive Review.Aging and disease · 2019Review
- The Impact of Infection in Pregnancy on Placental Vascular Development and Adverse Birth Outcomes.Frontiers in microbiology · 2019Review
- Molecular Principles of Intrauterine Growth Restriction in Plasmodium Falciparum Infection.Frontiers in endocrinology · 2019Review
- Bradykinin Sequestration byFrontiers in microbiology · 2018Article
- Human infectious diseases and risk of preeclampsia: an updated review of the literature.Infection · 2017Review
- Placental Malaria: A New Insight into the Pathophysiology.Frontiers in medicine · 2017Review
- Host Biomarkers Are Associated With Response to Therapy and Long-Term Mortality in Pediatric Severe Malaria.Open forum infectious diseases · 2016Article
- Experimental Malaria in Pregnancy Induces Neurocognitive Injury in Uninfected Offspring via a C5a-C5a Receptor Dependent Pathway.PLoS pathogens · 2015Article
- Malaria and immunity during pregnancy and postpartum: a tale of two species.Parasitology · 2015Review
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundPlacental malaria (PM) is a leading cause of maternal and infant mortality. Although the accumulation of parasitized erythrocytes (PEs) and monocytes within the placenta is thought to contribute to the pathophysiology of PM, the molecular mechanisms underlying PM remain unclear. Based on the hypothesis that excessive complement activation may contribute to PM, in particular generation of the potent inflammatory peptide C5a, we investigated the role of C5a in the pathogenesis of PM in vitro and in vivo. METHODOLOGY AND PRINCIPAL
findingsUsing primary human monocytes, the interaction between C5a and malaria in vitro was assessed. CSA- and CD36-binding PEs induced activation of C5 in the presence of human serum. Plasmodium falciparum GPI (pfGPI) enhanced C5a receptor expression (CD88) on monocytes, and the co-incubation of monocytes with C5a and pfGPI resulted in the synergistic induction of cytokines (IL-6, TNF, IL-1beta, and IL-10), chemokines (IL-8, MCP-1, MIP1alpha, MIP1beta) and the anti-angiogenic factor sFlt-1 in a time and dose-dependent manner. This dysregulated response was abrogated by C5a receptor blockade. To assess the potential role of C5a in PM, C5a plasma levels were measured in malaria-exposed primigravid women in western Kenya. Compared to pregnant women without malaria, C5a levels were significantly elevated in women with PM. CONCLUSIONS AND SIGNIFICANCE: These results suggest that C5a may contribute to the pathogenesis of PM by inducing dysregulated inflammatory and angiogenic responses that impair placental function.
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