Type I Pneumocytes

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... 

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... 

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 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. 

In the rat, the monoclonal antibody MEP-1 stained all cells lining the alveolar space, except the type II pneumocytes (Kasper et al. 1996). Double fluorescence staining employing type I cell-specific lectin BPA (Kasper et al. 1994) revealed the type I cell specificity. Immunoelectron microscopy confirmed this selective reaction of the MEP-1 antibody. The polyclonal anti pan-cathedrin antibody selectively decorated type I pneumocytes, alveolar macrophages and endothelial cells of large blood vessels. Caveolin is a selective marker of type I pneumocytes (Kasper and Reimann 1997). 

A limited munber of type I cell markers have been identified (Dobbs et al. 1988, 1999, Brody and Williams 1992, Danto et al. 1992, Christensen et al. 1993, Vanderbilt and Dobbs 1998). Dobbs et al. (1988) described rat type I cell 40kDa-protein, a glycoprotein defined by a monoclonal antibody raised against partially purified type I cells. In the lung it was localised to the apical plasma membrane of type I pneumocytes. The corresponding gene spans 35 kilobase pairs it contains 6 exons and at least 6 rat Identifier repetitive elements (Vanderbilt and Dobbs 1998). 

In the Syrian golden hamster, type-I pneumocytes were extremely sensitive for alveolar deposition of toxic substances as cadmium compounds (Thiede-MANN et al. 1992). 

In rats exposed to CdO for 3 days (18 h/d, 270 jig Cd/m sacrificed two days after the end of the exposure) necrosis of type-I pneumocytes and extensive proliferation of epithehal cells were most common, especially in the proximal region of the alveolar duct (Thiedemann et al. 1989, Paulini et al. 1992). 

Fig. 97. Membrane vesiculation (arrow) in a type I pneumocyte (left) and lamellar bodies in a type II pneumocyte (right) of an unmedicated male rat (No. 2573, block BNh 3767). Under pentobarbital anaesthesia (30 mg/kg), the animal was perfused from the abdominal aorta with 2.5 % glutaralde-hyde in 0.1 M sodium cacodylate buffer (pH 7.4). Postfixation with 1 % osmium te-troxide in sodium cacodylate buffer. Embedded in Epon 812 and sectioned at 50 nm. Lead citrate and uranyl acetate. Plate 2515...

Fig. no. Peroxisomes in an alveolar macrophage adjacent to a type I pneumocyte of a female rat (breeder Winkelmann, Borchen-Kirchborchen) which inhaled micronized deptro-pine citrate and isoprenaline hydrochloride Sa from a suspen-... 

FIGURE 1. A transmission electron micrograph of lung tissue illustrating attenuated type 1 pneu-mocytes (arrowheads), type II pneumocyte (arrow), and a pulmonary alveolar macrophage (PAM), a = alveolus c = capillary asterisk = platelet double arrowheads = capillary endothelium. The blood-air barrier consists of the type I pneumocyte, capillary endothelium, and the basement membrane separating these two cells. 

The histologic features of acute interstitial pneumonitis (AIP) are the various phases of DAD. Initially, an increase of capillary leukocytes including neutrophils, macrophages, and lymphocytes are seen. Within a day, interstitial edema becomes more evident and type I pneumocytes undergo type II metaplasia and become swollen. As the alveolar wall becomes necrotic, fibrin and cellular residue forms a layer of eosinophiUc material that lines the alveolar wall, the so-called hyaline membrane. Hyaline membranes are the defining feature of DAD. As the disease process progresses, polyps of organizing pneumonia develop and tend to replace the hyaline membranes (Fig. 4) (3,27,28). 

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