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

Ampawong S, Chaisri U, Viriyavejakul P, Prapansilp P, Grau GE, Turner GD, Pongponratn E - Malar. J. (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. am_sumate@hotmail.com.

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.

No MeSH data available.


Related in: MedlinePlus

Immunohistochemical staining for AQP-1 and -5 and bronchial cytokeratin. aBar chart comparing the degree of alveolar expression of AQP-1 and -5 and bronchial expression of cytokeratin in normal, non-PE, and PE-lung samples; photomicrographs of immunohistochemical staining of AQP-1 and -5 (localized on alveolar vessel and alveolar epithelium, respectively) and bronchial cytokeratin among normal (b, e, h), non-PE (c, f, i) and PE (d, g, j) lung samples
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Fig6: Immunohistochemical staining for AQP-1 and -5 and bronchial cytokeratin. aBar chart comparing the degree of alveolar expression of AQP-1 and -5 and bronchial expression of cytokeratin in normal, non-PE, and PE-lung samples; photomicrographs of immunohistochemical staining of AQP-1 and -5 (localized on alveolar vessel and alveolar epithelium, respectively) and bronchial cytokeratin among normal (b, e, h), non-PE (c, f, i) and PE (d, g, j) lung samples

Mentions: AQP-1 stained endothelial cell, AQP-5 staining pattern on alveolar/bronchial epithelial cells. These patterns are similar to those shown in previous publications. The expression levels of alveolar AQP-1 and -5 scoring and bronchial cytokeratin were not significantly different between severe malaria patients with or without PE and healthy subjects (Fig. 6). The maintenance of staining for pancytokeratin across groups allowed comparison of changes in other markers, given the potential for loss of immunoreactivity in blocks stored for some years.Fig. 6


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

Ampawong S, Chaisri U, Viriyavejakul P, Prapansilp P, Grau GE, Turner GD, Pongponratn E - Malar. J. (2015)

Immunohistochemical staining for AQP-1 and -5 and bronchial cytokeratin. aBar chart comparing the degree of alveolar expression of AQP-1 and -5 and bronchial expression of cytokeratin in normal, non-PE, and PE-lung samples; photomicrographs of immunohistochemical staining of AQP-1 and -5 (localized on alveolar vessel and alveolar epithelium, respectively) and bronchial cytokeratin among normal (b, e, h), non-PE (c, f, i) and PE (d, g, j) lung samples
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4595310&req=5

Fig6: Immunohistochemical staining for AQP-1 and -5 and bronchial cytokeratin. aBar chart comparing the degree of alveolar expression of AQP-1 and -5 and bronchial expression of cytokeratin in normal, non-PE, and PE-lung samples; photomicrographs of immunohistochemical staining of AQP-1 and -5 (localized on alveolar vessel and alveolar epithelium, respectively) and bronchial cytokeratin among normal (b, e, h), non-PE (c, f, i) and PE (d, g, j) lung samples
Mentions: AQP-1 stained endothelial cell, AQP-5 staining pattern on alveolar/bronchial epithelial cells. These patterns are similar to those shown in previous publications. The expression levels of alveolar AQP-1 and -5 scoring and bronchial cytokeratin were not significantly different between severe malaria patients with or without PE and healthy subjects (Fig. 6). The maintenance of staining for pancytokeratin across groups allowed comparison of changes in other markers, given the potential for loss of immunoreactivity in blocks stored for some years.Fig. 6

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Department of Tropical Pathology, Faculty of Tropical Medicine, Mahidol University, Bangkok, Thailand. am_sumate@hotmail.com.

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.

No MeSH data available.


Related in: MedlinePlus