Publication: A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
Issued Date
2015
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eng
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Mahidol University
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BioMed Central
Bibliographic Citation
Malaria Journal. Vol.14, (2015), 389
Suggested Citation
Sumate Ampawong, Urai Chaisri, Parnpen Viriyavejakul, Panote Prapansilp, Grau, Georges E, Turner, Gareth D. H., Emsri Pongponratn A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury. Malaria Journal. Vol.14, (2015), 389. doi:10.1186/s12936-015-0922-x Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/3080
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Title
A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
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Abstract
Background: The pathogenesis of pulmonary oedema (PE) in patients with severe malaria is still unclear. It has been
hypothesized that lung injury depends, in addition to microvascular obstruction, on an increased pulmonary capillary
pressure and altered alveolar-capillary membrane permeability, causing pulmonary fluid accumulation.
Methods: This study compared the histopathological features of lung injury in Southeast Asian patients (n = 43)
who died from severe Plasmodium falciparum malaria, and correlated these with clinical history in groups with or
without PE. To investigate the expression of mediators that may influence fluid accumulation in PE, immunohistochemistry
and image analysis were performed on controls and sub-sets of patient with or without PE.
Results: The expression of leukocyte sub-set antigens, bronchial interleukin (IL)-33, γ-epithelium sodium channel
(ENaC), aquaporin (AQP)-1 and -5, and control cytokeratin staining was quantified in the lung tissue of severe malaria
patients. Bronchial IL-33 expression was significantly increased in severe malaria patients with PE. Malaria patients with
shock showed significantly increased bronchial IL-33 compare to other clinical manifestations. Bronchial IL-33 levels
were positively correlated with CD68+ monocyte and elastase + neutrophil, septal congestion and hyaline membrane
formation. Moreover, the expression of both vascular smooth muscle cell (VSMC) and bronchial γ-ENaC significantly
decreased in severe malaria patients with PE. Both VSMC and bronchial γ-ENaC were negatively correlated with
the degree of parasitized erythrocyte sequestration, alveolar thickness, alveolar expansion score, septal congestion
score, and malarial pigment score. In contrast AQP-1 and -5 and pan cytokeratin levels were similar between groups.
Conclusions: The results suggest that IL-33 may play a role in lung injury during severe malaria and lead to PE. Both
VSMC and bronchial γ-ENaC downregulation may explain pulmonary fluid disturbances and participate in PE pathogenesis
in severe malaria patients.