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Type II cells

Normal lungs, however, produce a chemical substance referred to as pulmonary surfactant. Made by alveolar type II cells within the alveoli, surfactant is a complex mixture of proteins (10 to 15%) and phospholipids (85 to 90%), including dipalmitoyl phosphatidyl choline, the predominant constituent. By interspersing throughout the fluid lining the alveoli, surfactant disrupts the cohesive forces between the water molecules. As a result, pulmonary surfactant has three major functions ... [Pg.248]

Infant respiratory distress syndrome (IRDS), also known as hyaline membrane disease, is one of the most common causes of respiratory disease in premature infants. In fact, it occurs in 30,000 to 50,000 newborns per year in the U.S. — most commonly in neonates bom before week 25 of gestation. IRDS is characterized by areas of atelectasis, hemorrhagic edema, and the formation of hyaline membranes within the alveoli. IRDS is caused by a deficiency of pulmonary surfactant. Alveolar type II cells, which produce surfactant, do not begin to mature until weeks 25 to 28 of... [Pg.248]

FIGURE 34-2 Typical pattern of Alzheimer type II astrocytosis in frontal cortex of a 51-year-old cirrhotic patient who died in hepatic coma. Note astrocytes with large pale nucleus and margination of chromatin (large arrow). Doublets of Alzheimer type II cells frequently appear (open arrowhead). [Pg.597]

At both 3 and 6 months, there was a two- to threefold increase in volume density of alveolar Type II cells after 6 months, lungs had foci of pneumonia, suggesting a higher susceptibility to pulmonary... [Pg.504]

Collectins Alveolar type II cells and non-ciliated bronchiolar epithelial cells Bacterial and fungal cell walls and viruses Enhance phagocytosis of macrophages and neutrophils activating cells Cigarette smoke decreases the production of collectin [48] ozone decreases function [49]... [Pg.310]

Shelley, S.A., Paciga, J.E., and Balis, J.U., Lysozyme is an ozone-sensitive component of alveolar type II cell lamellar bodies, Biochim. Biophys. Acta. 1096, 4, 338, 1991. [Pg.324]

After intratracheal instillation of nickel chloride or nickel sulphate in rats, a modest inflammatory response with increased number of macrophages and polynuclear leucocytes was obtained, together with increased activities of lactate dehydrogenase and -glucuronidase in bronchoalveolar fluid [351]. More severe lesions were characterized by type II cell hyperplasia with epithelialization of alveoli, and in some animals, fibroplasia of the pulmonary interstitium. By inhalation in rats, the nickel salts produced chronic inflammation and degeneration of the bronchiolar epithelium [352, 353]. There was also atrophy of the olfactory epithelium and hyperplasia of the bronchial and mediastinal lymph nodes. Nickel sulphate also produced a low incidence of emphysema and fibrosis [353]. [Pg.213]

Ryan US, Ryan JW, Smith DS (1975) Alveolar type II cells studies on the mode of release of lamellar bodies. Tissue Cell 7(3) 587-599... [Pg.275]

Fehrenbach H (2001) Alveolar epithelial type II cell defender of the alveolus revisited. Respir Res 2(1 ) 33—46... [Pg.278]

Mason RJ (2006) Biology of alveolar type II cells. Respirology 11 SuppkS 12-S15... [Pg.278]

Rehan VK, Torday JS, Peleg S, Gennaro L, Vouros P, Padbury J, Rao DS, Reddy GS (2002) lAlpha,25-dihydroxy-3-epi-vitamin D3, a natural metabolite of 1 alpha,25-dihydroxy vitamin D3 production and biological activity studies in pulmonary alveolar type II cells. Mol Genet Metab 76(l) 46-56... [Pg.279]

Chen J, Chen Z, Narasaraju T, Jin N, Liu L (2004) Isolation of highly pure alveolar epithelial type I and type II cells from rat lungs. Lab Invest 84(6) 727-735 Erratum in Lab Invest 85(9) 1181 (2005)... [Pg.279]

Corti M, Brody AR, Harrison JH (1996) Isolation and primary culture of murine alveolar type II cells. Am J Respir Cell Mol Biol 14 309-315... [Pg.279]

Mulugeta S, Gray JM, Notarfrancesco KL, Gonzales LW, Koval M, Feinstein SI, Ballard PL, Fisher AB, Shuman H (2002) Identification of LBM180, a lamellar body limiting membrane protein of alveolar type II cells, as the ABC transporter protein ABC A3. J Biol Chem 277(25) 22147-22155... [Pg.280]

Balis JU, Bumgarner SD, Paciga JE, Paterson JF, Shelley SA (1984) Synthesis of lung surfactant-associated glycoproteins by A549 cells description of an in vitro model for human type II cell dysfunction. Exp Lung Res 6(3-4) 197-213... [Pg.281]

Lung compliance in vivo Ciliary beat assays in vitro Mucus level assays in vitro Alveolar Type II cell surfactant secretion assay in vitro Pharmacological profiling — binding or functional assays at receptors, enzymes, ion channels, transporters... [Pg.260]

Dietl, P., Haller, T., Mair, N., and Frick, M., Mechanisms of surfactantexocytosis in alveolar type II cells in vitro and in vivo, News Physiol. Sci., 16, 239-243, 2001. [Pg.284]

Straus, S. E., and Leirardo, M. J., 1999, Inherited human Caspase 10 mutations underhe defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoprohferative syndrome type II. Cell 98 47-58. [Pg.307]

Poelma DL, Zimmermann LJ, Scholten HH, et al. In vivo and in vitro uptake of surfactant lipids by alveolar type II cells and macrophages. Am J Physiol Lung Cell Mol Physiol 2002 283(3) L648-L654. [Pg.315]

Degenerative changes in Type 1 alveolar cells later replaced by Type II cells... [Pg.681]

The alveolar epithelium consists of so-called Type I and Type II cells. Type I cells cover over 90% of the alveolar surface, have a large surface, and are thin. Type II cells are larger in numbers but are small. Therefore, they cover only about 7% of the surface of the alveoli. Type II cells produce the phospholipids that make up the surfactant layer. [Pg.61]

The isolation and characterization of alveolar Type II cells which transform into alveolar Type I cells has been described, as weh as a monolayer culture of alveolar Type I cells [35,36]. [Pg.63]

The sequel to acute injury depends on the potency and concentration of the toxic agent and the duration of exposure. Potent gases produce a severe vascular reaction and alveolar flooding. The fluid prevents gaseous exchange, and death of the human or animal ensues. After acute mild nonlethal damage, excess fluid is removed and the resistant Type II cells proliferate and reline the alveoli. The cells subsequently differentiate into Type I cells. [Pg.6]

Ma LY, LaCagnin LB, Bowman L, et al. 1989. Carbon tetrachloride inhibits synthesis of pulmonary surfactant disaturated phosphatidylcholines and ATP production in alveolar type II cells. Acta Biochem Biophys 1003 136-144. [Pg.172]

An increase in lung lesions, as compared to controls, was observed in rats exposed to 0.7 mg nickel/m as nickel subsulfide for 78 weeks (6 hours/day, 5 days/week), followed by a 30-week observation period (Ottolenghi et al. 1974). The lung lesions included pneumonitis, atelectasis, bronchitis, bronchiectasis, and emphysema. Morphological alterations in alveolar macrophages (hyperplasia and lamellated material in the cytoplasm) were associated with impaired cellular function in rabbits exposed to 0.2 mg nickel/m as metallic nickel or nickel chloride for 8 months (Johansson and Camner 1986 Johansson et al. 1981). An increase in volume density of alveolar type II cells was also observed in rabbits exposed to 0.2 mg nickel/m as metallic nickel or nickel chloride for 1 month (Johansson and Camner 1986 Johansson et al. 1981). [Pg.52]

More severe respiratory effects (increased lung weight, increase in the accumulation of alveolar macrophages, increase in the density of type II cell volumes) were observed in rabbits exposed by inhalation to both nickel and trivalent chromium than in rabbits exposed to nickel only (Johansson et al. 1988b). [Pg.145]

White, J. F. Foley, R. R. Maronpot, and NT108 M. W. Anderson. Role of Clara cells and type II cells in the development of pulmonary tumors in rats and mice following exposure to a tobacco-specific nitrosamine. Exp Lung Res 1991 ... [Pg.345]


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See also in sourсe #XX -- [ Pg.646 ]




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