LPS, a kind of pro-inflammatory endotoxin from Gram-negative bacteria, can initiate inflammatory genes' expression and impair channel proteins' function in lung epithelial cells, resulting in pulmonary edema in ALI patients., ENaC is the primary executor for effective removal of excessive alveolar edema
through active Na + transport across the alveolar epithelium., LPS is reported to activate nuclear factor-?B signaling to inhibit SGK1 and ENaC expression in alveolar epithelial cells. In contrast, LXA4, an endogenously synthesized lipid, can effectively alleviate LPS-caused inflammation through priming AKT signaling and promoting ENaC expression., Great efforts have been devoted to the investigation of LXA4 protecting lung epithelial cells from LPS damage.
Histopathological examination in the current study focused on cellular intensity, cell type, perivascular mononuclear inflammation, alveolar edema
, bronchial damage and leukocyte infiltration.
(j) Blinded histopathological analysis for alveolar edema
, inflammatory infiltration, capillary congestion, and total histological scores.
But the term "pulmonary edema" creates a major confusion: many doctors imagine alveolar edema
, i.e, drowning of the patient.
The potential mechanisms include endothelial injury with alterations in endothelial permeability leading to interstitial and alveolar edema
, and intravascular sequestration of leukocytes.
On the 1st day after LPS injection, vast areas of alveolar edema
were detected in the lungs of newborn males and females.
Lung injury was evaluated according to the degree of alveolar edema
, interstitial edema, neutrophil infiltration, and hemorrhage.
This increased permeability leads to pulmonary interstitial and alveolar edema
. This protein-rich fluid floods the alveoli.
All histopathological changes were documented in each lung tissue, including intra-alveolar hemorrhage, alveolar edema
, disruption and congestion, and leukocyte infiltration.
When MCR was administered orally before LPS challenge (MCR-LPS group), inflammatory cell infiltration and alveolar wall thickening were markedly attenuated and alveolar edema
was reduced (Fig.
Qualitatively, all alterations characterizing the exudative phase of the histopathologic condition termed diffuse alveolar damage were identifiable, with intense congestion of the alveolar capillaries, marginated intracapillary neutrophils, necrosis of the alveolar epithelium, interstitial and alveolar edema
, hyaline membranes, and invasion of the alveoli by (mostly) mononucleate cells.
may be indistinguishable from hemorrhage or diffuse pneumonia.
During June 1-4, he became progressively hypoxemic and developed pulmonary alveolar edema