The influence of long-term (6 hours) immobilization stress on morphofunctional state of lung air-blood barrier was studied in experiments of the rats. It was shown that stress provoked the marked ultrastructural changes in the lungs, which were as follows: lung tissue oedema, pronounced thickening of lung air-blood barrier and its separate layers, edema-hemorrhagic syndrome, alveolar epithelial injury, disturbance of lung surfactant systems. Such a pathological complex may be designated as a "stress lung".
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This study describes a complex human in vitro model for evaluating anti-inflammatory drug response in the alveoli that may contribute to the reduction of animal testing in the pre-clinical stage of drug development. The model is based on the human alveolar epithelial cell line Arlo co-cultured with macrophages differentiated from the THP-1 cell line, creating a physiological biological microenvironment. To mimic the three-dimensional architecture and dynamic expansion and relaxation of the air-blood-barrier, they are grown on a stretchable microphysiological lung-on-chip.
View Article and Find Full Text PDFBackground: Seawater drowning (SWD) has been an escalating hazard in recent years. It can not only cause immediate death but can also inflict severe complications, such as acute lung injury (ALI), which greatly increases the mortality rate. Thus, investigating the mechanism of SWD induced lung injury and discovering effective treatments is of great importance.
View Article and Find Full Text PDFJ Aerosol Med Pulm Drug Deliv
December 2024
Department of Biomedical Research, University of Bern, Bern, Switzerland.
Histochem Cell Biol
November 2024
Hannover Medical School, Institute of Functional and Applied Anatomy, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Alveolar epithelial type I (AE1) cells with their wide spatial expansion form approximately 95% of the outer surface area of the air-blood barrier inside the lung. Serial block-face scanning electron microscopy (SBF-SEM) investigations led to the hypothesis that AE1 cell mitochondria are preferentially distributed as aggregates in those parts of AE1 cells that are located above connective tissue pillars between capillaries, thus not increasing the thickness of the diffusion distance for oxygen and carbon dioxide. Furthermore, it was hypothesised that postnatal development requires adapting the amount and distribution of mitochondria in AE1 cells.
View Article and Find Full Text PDFSci Rep
October 2024
Department of Emergency and Critical Care Medicine, Juntendo University Urayasu Hospital, Urayasu, Chiba, Japan.
Background The production of inflammatory cytokines is reportedly increased in patients with coronavirus disease 2019 (COVID-19), causing the migration of neutrophils and monocytes to lung tissues. This disrupts the air-blood barrier by damaging the bronchial epithelial and vascular endothelial cells. As multiorgan dysfunction in sepsis is considered to be partly caused by complement activation, which can cause lung injury in patients with COVID-19.
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