Fetal Alveolar Type II Cell Injury Induced by Short-term Exposure to Hyperoxia

2013 ◽  
Vol 20 (3) ◽  
pp. 300
Author(s):  
Hyeon-Soo Lee
Keyword(s):  
Cell Injury ◽  
Alveolar Type ◽  
Type Ii ◽  
Short Term ◽  
Alveolar Type Ii Cell ◽  
Short Term Exposure ◽  
Type Ii Cell

scholarly journals The cytoprotective role of DJ-1 and p45 NFE2 against human primary alveolar type II cell injury and emphysema

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Li Hui Tan ◽  
Karim Bahmed ◽  
Chih-Ru Lin ◽  
Nathaniel Marchetti ◽  
Sudhir Bolla ◽  
...  
Keyword(s):  
Cell Injury ◽  
Alveolar Type ◽  
Type Ii ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

Sublethal hydrogen peroxide inhibits alveolar type II cell surfactant phospholipid biosynthetic enzymes

1995 ◽  
Vol 268 (1) ◽  
pp. L129-L135 ◽  
Author(s):  
C. Crim ◽  
W. J. Longmore
Keyword(s):  
Cell Injury ◽  
Phospholipid Metabolism ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Reactive Oxygen Metabolites ◽  
Type Ii ◽  
Intracellular Atp ◽  
Alveolar Type Ii Cell ◽  
Atp Levels ◽  
Type Ii Cell

Alveolar type II cell injury by phagocytic cell-derived reactive oxygen metabolites represents a potential mechanism for the altered surfactant metabolism found in patients with the adult respiratory distress syndrome (ARDS). Previous studies demonstrated altered surfactant phospholipid metabolism after sublethal oxidant exposure. In this study, we measured intracellular ATP levels and the activities of several enzymes involved in surfactant phospholipid biosynthesis after sublethal H2O2 exposure of cultured rat alveolar type II cells. Intracellular ATP levels were reduced by 46.6% after exposure to 75 microM H2O2. The activity of CTP:phosphorylcholine cytidyltransferase was unchanged after H2O2 exposure when measured in whole cell homogenates. However, when measured in the microsomal fraction, cytidyltransferase activity significantly fell after exposure of type II cells to 75 microM H2O2. Activity in the cytosolic fractions remained unchanged. Similarly, microsomal cholinephosphotransferase was reduced after H2O2 exposure. We conclude that H2O2 decreases surfactant phosphatidylcholine biosynthesis independently of its ability to deplete intracellular ATP content. These deleterious effects may partially explain the diminished alveolar surfactant observed in patients with ARDS.

scholarly journals Covid-19 Interstitial Pneumonia: Histological and Immunohistochemical Features on Cryobiopsies

Respiration ◽  
2021 ◽  
pp. 369-379
Author(s):  
Claudio Doglioni ◽  
Claudia Ravaglia ◽  
Marco Chilosi ◽  
Giulio Rossi ◽  
Alessandra Dubini ◽  
...  
Keyword(s):  
Interstitial Pneumonia ◽  
Diffuse Alveolar Damage ◽  
Alveolar Type ◽  
Type Ii ◽  
Cell Hyperplasia ◽  
Nuclear Expression ◽  
Alveolar Type Ii Cell ◽  
Hyaline Membranes ◽  
Type Ii Cell ◽  
Phosphorylated Stat3

Background: The pathogenetic steps leading to Covid-19 interstitial pneumonia remain to be clarified. Most postmortem studies to date reveal diffuse alveolar damage as the most relevant histologic pattern. Antemortem lung biopsy may however provide more precise data regarding the earlier stages of the disease, providing a basis for novel treatment approaches. Objectives: To ascertain the morphological and immunohistochemical features of lung samples obtained in patients with moderate Covid-19 pneumonia. Methods: Transbronchial lung cryobiopsy was carried out in 12 Covid-19 patients within 20 days of symptom onset. Results: Histopathologic changes included spots of patchy acute lung injury with alveolar type II cell hyperplasia, with no evidence of hyaline membranes. Strong nuclear expression of phosphorylated STAT3 was observed in >50% of AECII. Interalveolar capillaries showed enlarged lumen and were in part arranged in superposed rows. Pulmonary venules were characterized by luminal enlargement, thickened walls, and perivascular CD4+ T-cell infiltration. A strong nuclear expression of phosphorylated STAT3, associated with PD-L1 and IDO expression, was observed in endothelial cells of venules and interstitial capillaries. Alveolar spaces macrophages exhibited a peculiar phenotype (CD68, CD11c, CD14, CD205, CD206, CD123/IL3AR, and PD-L1). Conclusions: Morphologically distinct features were identified in early stages of Covid-19 pneumonia, with epithelial and endothelial cell abnormalities different from either classical interstitial lung diseases or diffuse alveolar damage. Alveolar type II cell hyperplasia was a prominent event in the majority of cases. Inflammatory cells expressed peculiar phenotypes. No evidence of hyaline membranes and endothelial changes characterized by IDO expression might in part explain the compliance and the characteristic pulmonary vasoplegia observed in less-advanced Covid-19 pneumonia.

Quantitative Analysis of Alveolar Type II Cell Tumors in Mice by Whole Lung Serial and Step Sections

1989 ◽  
Vol 17 (4_part_2) ◽  
pp. 737-742 ◽  
Author(s):  
Sabine Rehm ◽  
Jerrold M. Ward
Keyword(s):  
Mouse Lung ◽  
Alveolar Type ◽  
Type Ii ◽  
Serial Sections ◽  
Feasible Method ◽  
Alveolar Type Ii Cell ◽  
Microscopic Lesion ◽  
Entire Lung ◽  
Type Ii Cell ◽  
Mouse Lungs

Alveolar type II cell tumors were induced transplacentally by intraperitoneal injection of pregnant C3H/HeNCr MTV– or Swiss Webster mice with N-nitrosoethylurea at a dose of 0.5 mmol/kg and 0.74 mmol/kg. At different time points after birth (1–32 weeks), the entire lungs from 40 of the male offspring were inflated with Bouin's fixative, separated into lobes, and sectioned at 5 μm serially to detect every microscopic lesion. Results were compared with those obtained from examining only every 10th, 20th, or a single mid-level section from the same material. On average, 150 serial sections were prepared per mouse lung. Initially, only purely solid/alveolar or purely tubulopapillary types were observed but with tumor progression, papillary structures developed within solid tumors resulting in mixed neoplasms. Analyzing mouse lungs in step sections of every 10th section (50–60 μm), 5/238 (2%) of the tumors were missed, in step sections of every 20th section (100–120 μm), 16/238 (7%) of the tumors were not detected and usually less than half of the tumors were seen in the single mid-level section. The approximate size of the neoplasms is indicated by the total number of sections per tumor. The dimensions of tumors evaluated with step sections of 10 or 20 were comparable to the size observed with serial sections. It is concluded that the evaluation of mouse lung tumors in steps of approximately 50 μm is basically equivalent to the study of serial sections and appears to be a feasible method to assess the complete incidence, histological type, and size of all proliferative processes throughout the entire lung.

scholarly journals Effects of Fas-Ligand Overexpression on Alveolar Type II Cell Growth Kinetics in Perinatal Murine Lungs

2010 ◽  
Vol 68 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Monique E de Paepe ◽  
Sheila A Haley ◽  
Zacharie Lacourse ◽  
Quanfu Mao
Keyword(s):  
Cell Growth ◽  
Growth Kinetics ◽  
Fas Ligand ◽  
Alveolar Type ◽  
Type Ii ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell ◽  
Cell Growth Kinetics

Cytotoxic effects of cigarette smoke extract on an alveolar type II cell-derived cell line

2001 ◽  
Vol 281 (2) ◽  
pp. L509-L516 ◽  
Author(s):  
Yuma Hoshino ◽  
Tadashi Mio ◽  
Sonoko Nagai ◽  
Hiroyuki Miki ◽  
Isao Ito ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Line ◽  
Cigarette Smoke ◽  
A549 Cells ◽  
Cigarette Smoke Extract ◽  
Alveolar Type ◽  
Type Ii ◽  
Cytotoxic Effects ◽  
Alveolar Type Ii Cell ◽  
Type Ii Cell

Injury of the alveolar epithelium by cigarette smoke is presumed to be an important process in the pathogenesis of smoking-related pulmonary diseases. We investigated the cytotoxic effects of cigarette smoke extract (CSE) on an alveolar type II cell-derived cell line (A549). CSE caused apoptosis at concentrations of 5% or less and necrosis at 10% or more. When CSE was exposed to air before application to A549 cells, the cytotoxic effects were attenuated. CSE caused cell death without direct contact with the cells. Acrolein and hydrogen peroxide, two major volatile factors in cigarette smoke, caused cell death in a similar manner. Aldehyde dehydrogenase, a scavenger of aldehydes, and N-acetylcysteine, a scavenger of oxidants and aldehydes, completely inhibited CSE-induced apoptosis. CSE and acrolein increased intracellular oxidant activity. In conclusion, apoptosis of alveolar epithelial cells may be one of the mechanisms of lung injury induced by cigarette smoking. This cytotoxic effect might be due to an interaction between aldehydes and oxidants present in CSE or formed in CSE-exposed cells.

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