Abstract
The main function of the lungs is oxygen transport from the atmosphere into the blood circulation, while it is necessary to keep the pulmonary tissue relatively free of pathogens. This is a difficult task because the respiratory system is constantly exposed to harmful substances entering the lungs by inhalation or via the blood stream. Individual types of lung cells are equipped with the mechanisms that maintain pulmonary homeostasis. Because of the clinical significance of acute respiratory distress syndrome (ARDS) the article refers to the physiological role of alveolar epithelial cells type I and II, endothelial cells, alveolar macrophages, and fibroblasts. However, all these cells can be damaged by lipopolysaccharide (LPS) which can reach the airspaces as the major component of the outer membrane of Gram-negative bacteria, and lead to local and systemic inflammation and toxicity. We also highlight a negative effect of LPS on lung cells related to alveolar-capillary barrier and their response to LPS exposure. Additionally, we describe the molecular mechanism of LPS signal transduction pathway in lung cells.
Highlights
From a histological point of view, the lung is a very complex organ
Administered LPS led to necrosis of alveolar macrophages and induction of acute lung injury (ALI) through P2X7 receptor pathway [52], which further supports the concept of TLR4-independent mechanisms of LPS action
LPS-induced inflammatory damage in the lungs is mediated by the receptor for advanced glycation end products (RAGE), which are expressed at high basal levels in alveolar type I (ATI) cells [66]
Summary
From a histological point of view, the lung is a very complex organ. The pulmonary epithelium consists of two major cell types—alveolar type I (ATI) cells and alveolar type II (ATII) cells, termed type I and type II pneumocytes. 2. Mechanism of LPS Signal Transduction Pathway in Lung Cells Lipopolysaccharide (LPS), named as endotoxin, is a part of the outer membrane of Gram-neAgsatwivaesbmacetnetriioan. LPS binds to a hydrophobic pocket of MD2 and directly cause dimerization of the TLR4-MD2 complex This triggers the recruitment of specific adaptor proteins to the intracellular domains and initiate a signaling cascade [38]. Hagar et al [46] have reported that LPS-activated caspase-11 causes an endotoxic shock in mice lacking TLR4 Another group studied the effect of accumulation mode particles in the presence of LPS on airway inflammation. Administered LPS led to necrosis of alveolar macrophages and induction of ALI through P2X7 receptor pathway [52], which further supports the concept of TLR4-independent mechanisms of LPS action
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