Simon O Owino

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Publications (2)6.68 Total impact

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    Article: C5a enhances dysregulated inflammatory and angiogenic responses to malaria in vitro: potential implications for placental malaria.
    Andrea Conroy, Lena Serghides, Constance Finney, Simon O Owino, Sanjeev Kumar, D Channe Gowda, W Conrad Liles, Julie M Moore, Kevin C Kain
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    ABSTRACT: Placental 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. Using 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. These results suggest that C5a may contribute to the pathogenesis of PM by inducing dysregulated inflammatory and angiogenic responses that impair placental function.
    PLoS ONE 02/2009; 4(3):e4953. · 4.09 Impact Factor
  • Article: Human immunodeficiency virus co-infection increases placental parasite density and transplacental malaria transmission in Western Kenya.
    Steven D Perrault, Jan Hajek, Kathleen Zhong, Simon O Owino, Moses Sichangi, Geoffrey Smith, Ya Ping Shi, Julie M Moore, Kevin C Kain
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    ABSTRACT: Plasmodium falciparum malaria and human immunodeficiency virus (HIV)-1 adversely interact in the context of pregnancy, however little is known regarding the influence of co-infection on the risk of congenital malaria. We aimed to determine the prevalence of placental and congenital malaria and impact of HIV co-infection on trans-placental malaria transmission in 157 parturient women and their infants by microscopy and by quantitative real-time polymerase chain reaction (PCR) in western Kenya. The prevalence of placental and cord blood infections were 17.2% and 0% by microscopy, and 33.1% and 10.8% by PCR. HIV co-infection was associated with a significant increase in placental parasite density (P < 0.05). Cord blood malaria prevalence was increased in co-infected women (odds ratio [OR] = 5.42; 95% confidence interval [CI] = 1.90-15.47) and correlated with placental parasite density (OR = 2.57; 95% CI = 1.80-3.67). A 1-log increase in placental monocyte count was associated with increased risk of congenital infection (P = 0.001) (OR = 48.15; 95% CI = 4.59-505.50). The HIV co-infected women have a significantly increased burden of placental malaria that increases the risk of congenital infection.
    The American journal of tropical medicine and hygiene 01/2009; 80(1):119-25. · 2.59 Impact Factor
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