BACKGROUND: The pathogenesis of @entity4 ( @entity4 ) in @entity1 with severe @entity311 is still unclear. It has been hypothesized that @entity651 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 @entity651 in Southeast Asian @entity1 (n  =  43) who died from severe @entity3964 @entity311 , and correlated these with clinical history in groups with or without @entity4 . To investigate the expression of mediators that may influence fluid accumulation in @entity4 , immunohistochemistry and image analysis were performed on controls and sub-sets of @entity1 with or without @entity4 . RESULTS: The expression of leukocyte sub-set antigens, bronchial interleukin (IL)-33, y-epithelium @entity1372 channel (ENaC), aquaporin ( @entity68035 , and control cytokeratin staining was quantified in the lung tissue of severe @entity311 @entity1 . Bronchial @entity6889 expression was significantly increased in severe @entity311 @entity1 with @entity4 . @entity311 @entity1 with shock showed significantly increased bronchial @entity6889 compare to other clinical manifestations. Bronchial @entity6889 levels were positively correlated with @entity469 + monocyte and elastase  +  neutrophil, septal congestion and hyaline membrane formation. Moreover, the expression of both vascular smooth muscle cell (VSMC) and bronchial y-ENaC significantly decreased in severe @entity311 @entity1 with @entity4 . Both VSMC and bronchial y-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 @entity68035 and pan cytokeratin levels were similar between groups. CONCLUSIONS: The results suggest that @entity6889 may play a role in @entity651 during severe @entity311 and lead to @entity4 . Both VSMC and bronchial y-ENaC downregulation may explain @entity358 and participate in @entity4 pathogenesis in severe @entity311 @entity1 .

A potential role for XXXX and y-epithelium @entity1372 channel in the pathogenesis of @entity1 @entity311 associated @entity651 .

@entity1 :: ('9606', 'Species') :: ['patients', 'patient'] @entity4 :: ('MESH:D004487', 'Disease') :: ['PE', 'pulmonary oedema'] @entity469 :: ('968', 'Gene') :: ['CD68'] @entity1372 :: ('MESH:D012964', 'Chemical') :: ['sodium'] @entity651 :: ('MESH:D055370', 'Disease') :: ['lung injury'] @entity358 :: ('MESH:D008171', 'Disease') :: ['pulmonary fluid disturbances'] @entity3964 :: ('5833', 'Species') :: ['Plasmodium falciparum'] @entity68035 :: ('358;362', 'Gene') :: ['AQP)-1 and -5', 'AQP-1 and -5'] @entity311 :: ('MESH:D008288', 'Disease') :: ['Malaria', 'malaria'] @entity6889 :: ('90865', 'Gene') :: ['IL-33']
@entity6889 :: (90865,Gene) :: ['interleukin-33']
