A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury

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, ca...

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Main Authors: Sumate Ampawong, Urai Chaisri, Parnpen Viriyavejakul, Panote Prapansilp, Grau, Georges E, Turner, Gareth D. H., Emsri Pongponratn
Other Authors: Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
Format: Article
Language:English
Published: 2017
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Online Access:https://repository.li.mahidol.ac.th/handle/123456789/3080
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spelling th-mahidol.30802023-03-31T00:48:24Z A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury Sumate Ampawong Urai Chaisri Parnpen Viriyavejakul Panote Prapansilp Grau, Georges E Turner, Gareth D. H. Emsri Pongponratn Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology Open Access article Aquaporin Gamma-epithelial sodium channel Interleukin-33 Leukocyte Malaria Pathogenesis Plasmodium falciparum Pulmonary oedema 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. 2017-11-08T03:13:21Z 2017-11-08T03:13:21Z 2017-11-08 2015 Research Article Malaria Journal. Vol.14, (2015), 389 10.1186/s12936-015-0922-x https://repository.li.mahidol.ac.th/handle/123456789/3080 eng Mahidol University BioMed Central application/pdf
institution Mahidol University
building Mahidol University Library
continent Asia
country Thailand
Thailand
content_provider Mahidol University Library
collection Mahidol University Institutional Repository
language English
topic Open Access article
Aquaporin
Gamma-epithelial sodium channel
Interleukin-33
Leukocyte
Malaria
Pathogenesis
Plasmodium falciparum
Pulmonary oedema
spellingShingle Open Access article
Aquaporin
Gamma-epithelial sodium channel
Interleukin-33
Leukocyte
Malaria
Pathogenesis
Plasmodium falciparum
Pulmonary oedema
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
description 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.
author2 Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
author_facet Mahidol University. Faculty of Tropical Medicine. Department of Tropical Pathology
Sumate Ampawong
Urai Chaisri
Parnpen Viriyavejakul
Panote Prapansilp
Grau, Georges E
Turner, Gareth D. H.
Emsri Pongponratn
format Article
author Sumate Ampawong
Urai Chaisri
Parnpen Viriyavejakul
Panote Prapansilp
Grau, Georges E
Turner, Gareth D. H.
Emsri Pongponratn
author_sort Sumate Ampawong
title A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
title_short A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
title_full A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
title_fullStr A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
title_full_unstemmed A potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
title_sort potential role for interleukin‑33 and γ‑epithelium sodium channel in the pathogenesis of human malaria associated lung injury
publishDate 2017
url https://repository.li.mahidol.ac.th/handle/123456789/3080
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