Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury

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.

Short-Term versus Long-Term Culture of A549 Cells for Evaluating the Effects of Lipopolysaccharide on Oxidative Stress, Surfactant Proteins and Cathelicidin LL-37

“…It has been shown that LPS can modulate surfactant protein levels in alveolar epithelial cells [2]. In previous studies, SP-A gene expression increased in A549 cells and mice lungs challenged by LPS, while SP-D synthesis remained unaffected by endotoxin [7,16,72].…”

“…ATII cells are considered to be the progenitor population of alveoli and play an important role in innate immune responses of the lungs [2]. Thus, these cells and their proper functions are essential for maintaining lung integrity and homeostasis.…”

“…Similarly, Tang et al [36] tested the effect of serum concentration on the viability of A549 cells and they observed LPS-induced cell death only in the presence of serum at a minimum concentration of 5%. One possible explanation could be that A549 cells do not express CD14 protein [35], an important part of LPS signal transduction pathway [2]. Therefore, there is a need for serum as a rich source of soluble CD14 [35,37].…”

“…ATI cells are large, flat cells which cover approximately 90% of the alveolar surface, and their main roles are gas exchange and maintenance of fluid balance. A major function of small cuboidal ATII cells is the production of pulmonary surfactant, which is fundamental for preventing of alveolar collapse by reducing surface tension at the end of expiration, and plays an important role in the local pulmonary defense mechanisms in which mainly surfactant proteins (SPs) are involved [1,2]. ATII cells are also the main source of endogenous antimicrobial peptides; among them is cathelicidin hCAP18/LL-37 [3,4].…”

Utilização Do Brief Medication Questionnaire Na Avaliação Da Adesão De Pacientes Iniciantes Em Terapia Antirretroviral

“…No dano pulmonar agudo induzido por LPS, o mecanismo de resposta mais comum é a via receptor de membrana CD14, no qual gera uma cascata via MyD88 dependente até a fosforilação do Fator Nuclear Kappa B (NFkB), que é uma via de sinalização nuclear para a produção de proteínas inflamatórias, tais como IL-1, IL-6, IL-8 e TNF-alpha (Nova et al, 2019) como demonstrado na Figura 01.…”