Type 1 pneumocytes

Noncoated omega, smooth-coated, or flask-shaped invaginations (35) were initially discovered by Palade et al. (38). They are called caveolae and have a maximal diameter of 70 nm. They start from the plasmalemma and have a neck-like structure. By electron microscopy, caveolae can be distinguished from clathrin-coated pits because they are not associated with an electron-dense cytoplasmic coat. Caveolae are abundantly present in endothelial and smooth muscle cells, but are also present in epithelial cells, adipocytes, fibroblasts, type 1 pneumocytes, and striated muscle cells (39). Caveolae are coated with proteins that belong to the family of caveolins [caveolin-1 (alpha, lbeta), caveolin-2(alpha, beta, gamma), and caveolin-3 (39)], but other proteins, such as flotillin-1, MALI, and MEC-2/stomatin proteins, may also be involved in caveolae formation (40). 

Fig. 96. Prominent microtubules in a cell process of a type 1 pneumocyte from a female white rat (No. 4 breeder Winkelmann, Borchen-Kirchborchen), which inhaled 10 mg powdered aluminium/m 4 h per day, 5 days per week from August 16 to October 27, 1967 for a total of 51 days. Fixed on January 15, 1968 under methitural anaesthesia by intratracheal instillation of 2.5 % glutaralde-hyde in phosphate buffer (pH 7.4) before opening the thorax. Postfixation with 1 % osmium tetroxide in phosphate buffer (pH 7.4). Contrasted en bloc for 12 h with 0.5 % uranyl acetate in 70 % ethanol. Embedded in a 2 8 mixture of methyl and butyl methacrylate. Sectioned at 50 nm. Lead citrate after Reynolds (1963). Plate 38/02...

Hackett and Sunderman 1968). Great enlargement of the nuclei and nucleoli was observed two to six days. The cytoplasm contained prominent arrays of rough endoplasmic reticulum, as well as increased numbers of free ribosomes and mitochondria. In some of the type 1 pneumocytes, the endoplasmic reticulum was distended with flocculent osmiophiUc material. Abundant Golgi zones were present. Multivesicular bodies were found two and four days after Ni(CO)4 appUcation. They were usually surrounded by a single membrane. 

Complement (C3a, C5a) Macrophages, type II pneumocytes and fibroblasts Microbes Opsinization by phagocytes and chemotaxis Increased activity after exposure to LPS and allergens ozone, diesel, cigarette [23, 28]... 

It is commonly known that lipids, carbohydrates, and glycolipids are present in the Golgi apparatus (27). The determination of the components that react with the ZIO mixture was carried out by removing each component from tissues before incubation in the ZIO mixture. After lipid extraction by acetone (14), chloroform-methanol (15), or propylene oxide (27), no osmium-zinc precipitates could be detected in structures that normally reacted with ZIO. Blumcke et al. (15) summarized the nature of the lipids that react with the ZIO mixture as follows lipids and lipoproteins of cell membranes, neutral fat droplets (41), and lipid globules of type II pneumocytes and alveolar macrophages were, however, not as electron dense as the normally reactive lamellae containing highly unsaturated fatty acids. 

Blumcke WD, Kessler HR, Niedorf NH, Veith FJ. Ultrastructure of lamellar bodies of type II Pneumocytes after osmium-zinc impregnation. J Ultrastruct Res 1973 42 417-433. 

The cellular uptake appears to be a passive process, the cellular distribution being dependent on cell type. In cultured pneumocytes, the cell membrane was... 

The human alveolar epithelium consists of two cell types type I (alveolar epithelial type I [ATI], pneumocyte I) and type n (alveolar epithelial type II... 

ATII cells, when plated on permeable supports or plastics under appropriate culture conditions, acquire features of type I cell-like phenotype and morphology [30, 57, 80], Although isolation of ATI pneumocytes from rat lungs has recently been reported with some success [28, 48, 81], development of confluent ATI cell monolayer with electrically tight characteristics has not been reported yet. It should be noted that unlike many other cells in primary culture, AEC exhibits generally a very limited proliferation profile and is therefore not suitable for passaging. Thus, a new preparation of cells has to be used for each data set, which drives the costs up tremendously, and a reliable normalisation scheme of data observed from each set of cell preparations is needed. 

Fehrenbach H, Schmiedl A, Wahlers T, Hirt SW, Brasch F, Riemann D, Richter J (1995) Morphometric characterisation of the fine structure of human type II pneumocytes. Anat Rec 243(1 ) 49-62... 

Kasper M, Reimann T, Hempel U, Wenzel KW, Bierhaus A, Schuh D, Dimmer V, Haroske G, Muller M (1998) Loss of caveolin expression in type I pneumocytes as an indicator of subcellular alterations during lung fibrogenesis. Histochem Cell Biol 109(1) 41—48... 

Bingle L, Bull TB, Fox B, Guz A, Richards RJ, Tetley TD (1990) Type II pneumocytes in mixed cell culture of human lung a light and electron microscopic study. Environ Health Perspect 85 71-80... 

Caveloae are particularly abundant, accounting for 30-70% of the plasma membrane in differentiated epithelial (e.g., pneumocytes) and endothelial cells, fibroblasts, smooth muscle cells, and adipocytes. Indeed there is a general trend for caveolin induction in differentiated cell types. Adipose tissue is replete with caveolae, and caveolin mRNA and protein are strongly induced during differentiation of 3T3-L1 preadipocytes (fibroblasts) to adipocytes [10], While... 

In animals, acute oral exposure to doses of 4,000 mg/kg has been observed to cause respiratory edema, atelectasis and hemorrhage (Gould and Smuckler 1971). This is accompanied by marked disruption of subcellular structure in most pulmonary cell types, including granular pneumocytes, capillary endothelial cells and Clara cells (Boyd et al. 1980 Gould and Smuckler 1971 Hollinger 1982). It has been shown that Clara cells were most severely injured because they are the most active in metabolic activation of carbon tetrachloride. Injury to capillary endothelial cells is dose-... 

In many cell types it is feasible to deliver nucleic acids and genes by a variety of methods when the cells are grown in tissue culture (Table 58.1). Nonetheless, some cells, such as pneumocytes and neurons, are not readily isolated from humans and do not grow well in vitro. Furthermore, for many diseases it is essential to alter the phenotype of a significant proportion of the total cell population, making ex vivo gene therapy of limited use. 

Phospholipid that is the major component of Tung surfactant, and the syndrome caused by its deficiency Dipalmitoylphosphatidylcholine (DPPC, also called dipalmitoyllecithin, DPPL) is the major lipid component of lung surfactant. It is made and secreted by type II granular pneu-mocytes. Insufficient surfactant production causes respiratory distress syndrome, which can occur in preterm infants or adults whose surfactant-producing pneumocytes have been damaged or destroyed. 

At the distal respiratory site, the alveolar epithelial cell layer is much flatter (0.1 -0.5 pm) and composed of two major cell types, squamous type I and agranular type II pneumocytes. Type I pneumocytes are non-phagocytic and highly flattened cells with broad and thin extensions. They occupy -95 % of the alveolar luminal surface, although they are less numerous than type II cells. The remaining surface is occupied by type II pneumocytes, which have blunt microvilli and contain multivesicular bodies [3, 11]. 

Type I pneumocytes, joined with endothelial cells by fused basement membranes, offer a very short airways-blood pathway for the diffusion of gases and drug molecules. They are known to contain numerous endocytotic vesicles which play an important role in the absorption process of proteins and transcellular movement of transporters [12, 13]. The functions of type II pneumocytes are well studied and include... 

Hydrophilic surfactant proteins A (SP-A) and D (SP-D), secreted by type II pneumocytes, interact specifically with a wide range of microorganisms and play important roles in the innate, natural defense system of the lung [16]. Both mRNA and protein levels of SP-A and SP-D increase dramatically in response to lung infection, injury and endotoxin challenge [17]. Type II pneumocytes also express class II major histocompatibility complex (MHC) antigens and intracellular adhesion molecule (ICAM-1), which may facilitate pulmonary immune responses [15]. 

Helliwell, P.A., D. Meredith, C.A. Boyd, J.R. Bronk, N. Lister, and P.D. Bailey. 1994. Tripeptide transport in rat lung. Biochim. Biophys. Acta 1190 430-434. Meredith, D., and C.A. Boyd. 1995. Dipeptide transport characteristics of the apical membrane of rat lung type II pneumocytes. Am.]. Physiol. 269 L137-L143. 

Type-I pneumocytes thin cells offering a very short airways-blood path length for the diffusion of gases and drug molecules. Type-I pneumocytes occupy about 93% of the surface area of the alveolar sacs, despite being only half as abundant as type-II cells. 

Type-II pneumocytes cuboidal cells that store and secrete pulmonary surfactant. 

All the major cell types (epithelial, endothelial, smooth muscle cells, pneumocytes, chondrocytes, fibroblasts) capable of producing connective tissues (e.g. cartilage, basement membrane, parenchymal stroma) are susceptible to oxidative injury in vitro [29- 33], and over the past decade the mechanism(s) of oxidative stress to these cell types has been the focus of intense research. Unfortunately, few of these studies have been specifically extended to examine the biochemical evidence for oxidative injury to connective tissue producing cells in vivo [34], Our most recent work has concentrated on determining the precise biochemical footprints of oxidative injury found within chondrocytes (also colonic epithelial cells) and attempting to correlate the presence or absence of these oxidative-injury markers seen in vitro with inflamed material from animal models and human pathological material. 

Type I pneumocytes make up most of the epithelial surface. It is the large, thin, type I pneumocytes that are the primary site of pulmonary protein absorption. The type II pneumocytes, lying in niches between type I cells, are the main source of surfactants and also replace type I cells as they undergo apoptosis (programmed cell death) after about 120 days. 

Three patients with busulfan-induced interstitial pneumonitis each had circulating immune complexes and alveolitis, and histology demonstrated consistent abnormalities of type I pneumocytes and depletion of type II pneumocytes (7). 

Adult rats were exposed to different concentrations of n-hexane and lung tissue was then examined. The direct toxic effect to pneumocytes could be demonstrated as definite regressive alterations, such as fatty generation and change of lamellar bodies of type II pneumocytes as well as increased detachment of cells. After chronic inhalation of solvents, conspicuous aggregation of lamellar discharge material of type II pneumocytes can be seen and, probably as a result of an irritated fat metabolism, there were large lysosome-like bodies with densely packed lipid material in type I pneumocytes. 

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