The phospholipids of rabbit type II alveolar epithelial cells: Comparison with lung lavage, lung tissue, alveolar macrophages, and a human alveolar tumor cell line

Lipids ◽  
1977 ◽  
Vol 12 (5) ◽  
pp. 438-442 ◽  
Author(s):  
S. A. Rooney ◽  
L. L. Nardone ◽  
D. L. Shapiro ◽  
E. K. Motoyama ◽  
L. Gobran ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Tumor Cell ◽  
Cell Line ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Tumor Cell Line ◽  
Lung Lavage ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial

A continuous tumor-cell line from a human lung carcinoma with properties of type II alveolar epithelial cells

1976 ◽  
Vol 17 (1) ◽  
pp. 62-70 ◽  
Author(s):  
Michael Lieber ◽  
George Todaro ◽  
Barry Smith ◽  
Andras Szakal ◽  
Walter Nelson-Rees
Keyword(s):  
Epithelial Cells ◽  
Tumor Cell ◽  
Cell Line ◽  
Lung Carcinoma ◽  
Human Lung ◽  
Tumor Cell Line ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Human Lung Carcinoma

scholarly journals Characterization of Early Stages of Human Alveolar Infection by the Q Fever AgentCoxiella burnetii

2019 ◽  
Vol 87 (5) ◽  
Author(s):  
Amanda L. Dragan ◽  
Richard C. Kurten ◽  
Daniel E. Voth
Keyword(s):  
Epithelial Cells ◽  
Lung Tissue ◽  
Alveolar Macrophages ◽  
Human Lung ◽  
Q Fever ◽  
Cell Types ◽  
Alveolar Epithelial Cells ◽  
Human Lung Tissue ◽  
Content Type ◽  
Alveolar Epithelial

ABSTRACTHuman Q fever is caused by the intracellular bacterial pathogenCoxiella burnetii. Q fever presents with acute flu-like and pulmonary symptoms or can progress to chronic, severe endocarditis. After human inhalation,C. burnetiiis engulfed by alveolar macrophages and transits through the phagolysosomal maturation pathway, resisting the acidic pH of lysosomes to form a parasitophorous vacuole (PV) in which to replicate. Previous studies showed thatC. burnetiireplicates efficiently in primary human alveolar macrophages (hAMs) inex vivohuman lung tissue. AlthoughC. burnetiireplicates in most cell typesin vitro, the pathogen does not grow in non-hAM cells of human lung tissue. In this study, we investigated the interaction betweenC. burnetiiand other pulmonary cell types apart from the lung environment.C. burnetiiformed a prototypical PV and replicated efficiently in human pulmonary fibroblasts and in airway, but not alveolar, epithelial cells. Atypical PV expansion in alveolar epithelial cells was attributed in part to defective recruitment of autophagy-related proteins. Further assessment of theC. burnetiigrowth niche showed that macrophages mounted a robust interleukin 8 (IL-8), neutrophil-attracting response toC. burnetiiand ultimately shifted to an M2-polarized phenotype characteristic of anti-inflammatory macrophages. Considering our findings together, this study provides further clarity on the uniqueC. burnetii-lung dynamic during early stages of human acute Q fever.

scholarly journals Cysteine proteinases in bronchoalveolar epithelial cells and lavage fluid of rat lung.

1991 ◽  
Vol 39 (4) ◽  
pp. 461-468 ◽  
Author(s):  
Y Ishii ◽  
Y Hashizume ◽  
T Watanabe ◽  
S Waguri ◽  
N Sato ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophages ◽  
Cathepsin B ◽  
Light And Electron Microscopy ◽  
Lavage Fluid ◽  
Alveolar Epithelial Cells ◽  
Type Ii ◽  
Mature Form ◽  
Alveolar Epithelial ◽  
Cathepsin H

We examined the presence of cathepsins B, H, and L in bronchoalveolar epithelial cells, including alveolar macrophages, and in bronchoalveolar lavage fluid (BALF), using immunocytochemistry and immunoblotting. By light and electron microscopy, immunoreactivity for cathepsins B, H, and L was detected in lysosomes of ciliated and non-ciliated epithelial cells of bronchi and bronchioles, and in macrophages. Immunodeposits for cathepsin H only were demonstrated in lamellar bodies of Type II alveolar epithelial cells, suggesting the cosecretion of surfactants and cathepsin H from the cells into the alveolar space. By immunoblotting, cathepsins B and H were found to be present in BALF. To further investigate the origin of these enzymes in BALF, alveolar macrophages obtained from BALF were cultured for 6 hr in a serum-free medium. Immunoblotting revealed that protein bands corresponding to the pro-form and mature form of cathepsin B and the mature form of cathepsin H were present in the culture medium. From these results, the presence of cathepsins B and H in BALF can be explained by the fact that cathepsin B is secreted from alveolar macrophages and cathepsin H is secreted mainly with surfactants from Type II cells and also from macrophages.

Cellular uptake of albumin from lungs of anesthetized rabbits

1995 ◽  
Vol 269 (4) ◽  
pp. L453-L462 ◽  
Author(s):  
R. H. Hastings ◽  
H. G. Folkesson ◽  
V. Petersen ◽  
R. Ciriales ◽  
M. A. Matthay
Keyword(s):  
Epithelial Cells ◽  
Cellular Uptake ◽  
Alveolar Macrophages ◽  
Colloidal Gold ◽  
Soluble Protein ◽  
Alveolar Epithelial Cells ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Protein Clearance

Resolution of alveolar edema depends on clearance of serum protein, as well as liquid from the alveolar space. Protein clearance is slower than liquid clearance and may take days to weeks. Our earlier studies presented evidence for the importance of paracellular removal of soluble protein from the air spaces. However, long-term protein clearance may also depend on uptake by alveolar epithelial cells or macrophages. This study examined cellular uptake of soluble human albumin and insoluble colloidal gold-albumin from the lungs of anesthetized rabbits. Native albumin was endocytosed by both alveolar type I and type II cells and appeared in vesicles and endosomes. Neither cell type took up colloidal gold-albumin over periods as long as 8 h. Alveolar macrophages took up native albumin and colloidal gold-albumin to a greater extent and more rapidly than alveolar epithelial cells. The tracer proteins were found in vesicles, endosomes, and phagolysosomes. Similarly, cultured alveolar macrophages took up native albumin more rapidly than cultured type II cells. Thus macrophages may be important in clearing precipitated protein from the air spaces, and they may have a role in completing the clearance of soluble protein. The potential for transepithelial transport of soluble alveolar protein exists, but based on this work and our prior studies, it appears to be a low-capacity pathway.

Proinflammatory response of alveolar epithelial cells is enhanced by alveolar macrophage-produced TNF-α during pulmonary ischemia-reperfusion injury

2007 ◽  
Vol 293 (1) ◽  
pp. L105-L113 ◽  
Author(s):  
Ashish K. Sharma ◽  
Lucas G. Fernandez ◽  
Alaa S. Awad ◽  
Irving L. Kron ◽  
Victor E. Laubach
Keyword(s):  
Epithelial Cells ◽  
Alveolar Macrophage ◽  
Alveolar Macrophages ◽  
Ischemia Reperfusion ◽  
Alveolar Epithelial Cells ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Alveolar Epithelial ◽  
Tnf Α

Pulmonary ischemia-reperfusion (IR) injury entails acute activation of alveolar macrophages followed by neutrophil sequestration. Although proinflammatory cytokines and chemokines such as TNF-α and monocyte chemoattractant protein-1 (MCP-1) from macrophages are known to modulate acute IR injury, the contribution of alveolar epithelial cells to IR injury and their intercellular interactions with other cell types such as alveolar macrophages and neutrophils remain unclear. In this study, we tested the hypothesis that following IR, alveolar macrophage-produced TNF-α further induces alveolar epithelial cells to produce key chemokines that could then contribute to subsequent lung injury through the recruitment of neutrophils. Cultured RAW264.7 macrophages and MLE-12 alveolar epithelial cells were subjected to acute hypoxia-reoxygenation (H/R) as an in vitro model of pulmonary IR. H/R (3 h/1 h) significantly induced KC, MCP-1, macrophage inflammatory protein-2 (MIP-2), RANTES, and IL-6 (but not TNF-α) by MLE-12 cells, whereas H/R induced TNF-α, MCP-1, RANTES, MIP-1α, and MIP-2 (but not KC) by RAW264.7 cells. These results were confirmed using primary murine alveolar macrophages and primary alveolar type II cells. Importantly, using macrophage and epithelial coculture methods, the specific production of TNF-α by H/R-exposed RAW264.7 cells significantly induced proinflammatory cytokine/chemokine expression (KC, MCP-1, MIP-2, RANTES, and IL-6) by MLE-12 cells. Collectively, these results demonstrate that alveolar type II cells, in conjunction with alveolar macrophage-produced TNF-α, contribute to the initiation of acute pulmonary IR injury via a proinflammatory cascade. The release of key chemokines, such as KC and MIP-2, by activated type II cells may thus significantly contribute to neutrophil sequestration during IR injury.

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