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C5a enhances dysregulated inflammatory and angiogenic responses to malaria in vitro: potential implications for

Andrea Conroy1, Lena Serghides, Constance Finney

  • 1McLaughlin-Rotman Centre for Global Health, Toronto General Hospital, McLaughlin Centre for Molecular Medicine, University of Toronto, Toronto, Ontario, Canada.

Plos One
|March 25, 2009
PubMed
Abstract

Insights

Complement component 5a (C5a) may drive placental malaria (PM) pathogenesis. Elevated C5a levels in pregnant women with PM suggest its role in impairing placental function through inflammatory and angiogenic responses.

Area of Science:

  • Immunology
  • Obstetrics
  • Infectious Diseases

Background:

  • Placental malaria (PM) significantly contributes to maternal and infant mortality.
  • The precise molecular mechanisms of PM pathophysiology, particularly the role of monocytes and parasitized erythrocytes, are not fully understood.
  • Excessive complement system activation, specifically C5a generation, is hypothesized to be involved in PM.

Purpose of the Study:

  • To investigate the role of C5a in the pathogenesis of placental malaria.
  • To elucidate the molecular mechanisms by which C5a influences placental inflammation and function.

Main Methods:

  • In vitro studies using primary human monocytes and Plasmodium falciparum components.
  • Assessment of C5 activation by parasitized erythrocytes.
  • Measurement of cytokine, chemokine, and anti-angiogenic factor production.
  • In vivo analysis of C5a plasma levels in pregnant women with and without PM in Kenya.

Main Results:

  • Parasitized erythrocytes activated complement component C5.
  • Plasmodium falciparum GPI enhanced C5a receptor expression on monocytes.
  • Co-incubation with C5a and pfGPI synergistically induced inflammatory cytokines, chemokines, and sFlt-1.
  • C5a receptor blockade abrogated these dysregulated responses.
  • Significantly elevated C5a plasma levels were observed in women with PM compared to uninfected pregnant women.

Conclusions:

  • C5a contributes to placental malaria pathogenesis.
  • C5a induces dysregulated inflammatory and angiogenic responses.
  • These C5a-mediated responses impair placental function, highlighting C5a as a potential therapeutic target.

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