Overexpression of Sphingosine Kinase-1 and Sphingosine-1-Phosphate Receptor-3 in Severe Plasmodium falciparum Malaria with Pulmonary Edema.

Pulmonary edema (PE) is a major cause of pulmonary manifestations of severe Plasmodium falciparum malaria and is usually associated with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The sphingosine kinase-1 (SphK-1)/sphingosine-1-phosphate receptor-3 (S1PR-3) pathway has r...

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Published in:BioMed Research International pp. 1 - 8
Main Authors: Viriyavejakul, Parnpen, Punsawad, Chuchard
Format: pictorial research tables/charts Journal Article
Published: Wiley-Blackwell 2/26/2020
Online Access:View this record in EBSCOhost
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      jtl: BioMed Research International
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      dt: 2/26/2020
      pid: 480
      pub: Wiley-Blackwell
      place: Malden, Massachusetts
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        10.1155/2020/3932569
        141933583
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        atl: Overexpression of Sphingosine Kinase-1 and Sphingosine-1-Phosphate Receptor-3 in Severe Plasmodium falciparum Malaria with Pulmonary Edema.
      aug:
        au:
          Viriyavejakul, Parnpen
          Punsawad, Chuchard
        affil: Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, Bangkok 10400, Thailand
      sug:
        subj:
          Glycols Metabolism
          Protein Kinases Metabolism
          Receptors, Cell Surface Metabolism
          Gene Expression
          Malaria Complications
          Severity of Illness
          Pulmonary Edema Pathology
          Human
          Immunohistochemistry
          Malaria Mortality
          Epithelial Cells Metabolism
          Macrophages Metabolism
      ab: Pulmonary edema (PE) is a major cause of pulmonary manifestations of severe Plasmodium falciparum malaria and is usually associated with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). The sphingosine kinase-1 (SphK-1)/sphingosine-1-phosphate receptor-3 (S1PR-3) pathway has recently been reported to affect the pathogenesis of lung injury, but the expression of these proteins in the lungs of severe P. falciparum malaria patients has not been investigated. The cellular expression of SphK-1 and S1PR-3 in lung tissues from autopsied patients with P. falciparum malaria was investigated using immunohistochemistry (IHC). Lung tissues from patients who died of severe P. falciparum malaria were classified into two groups based on histopathological findings: those with PE (18 patients) and those without PE (non-PE, 19 patients). Ten samples of normal lung tissues were used as the control group. The protein expression levels of SphK-1 and S1PR-3 were significantly upregulated in endothelial cells (ECs), alveolar epithelial cells, and alveolar macrophages (AMs) in the lungs of severe P. falciparum malaria patients with PE compared to those in the non-PE and control groups (all p < 0.001). In addition, the SphK-1 and S1PR-3 expression levels were significantly positively correlated in pulmonary ECs ( r s = 0.922 , p < 0.001), alveolar epithelial cells ( r s = 0.995 , p < 0.001), and AMs ( r s = 0.969 , p < 0.001). In conclusion, both the SphK-1 and S1PR-3 proteins were overexpressed in the lung tissues of severe P. falciparum malaria patients with PE, suggesting that SphK-1 and S1PR-3 mediate the pathogenesis of PE in severe malaria. Targeting the regulation of SphK-1 and/or S1PR-3 may be an approach to treat pulmonary complications in severe P. falciparum patients.
      pubtype: Academic Journal
      doctype:
        pictorial
        research
        tables/charts
        Journal Article
      ougenre: Article
    language: English
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