Altered regulation of surfactant phospholipid and protein A during acute pulmonary inflammation.

Biochemical changes in the pulmonary surfactant system caused by exposure to toxicants are often accompanied by an influx of inflammatory cells into the lungs. We have investigated the possibility that the inflammatory and surfactant biochemical effects might be connected. Co-treatment with dexamethasone, a synthetic anti-inflammatory glucocorticoid, mitigated the increases in free cells and total intracellular surfactant phospholipid normally seen in animals given silica alone, suggesting a relationship between the free cell population of the alveoli and the surfactant system during alveolitis.

Detection of candidates for cancer cell motility inhibitory protein in the Dunning adenocarcinoma model.

The more differentiated components of a primary tumor may produce substances that reduce the growth rate and metastatic potential of more aggressive components. In the Dunning R-3327 prostatic adenocarcinoma model, cancer cell motility is required for metastatic potential. Medium conditioned by the non-motile, non-metastatic G subline contains proteins of molecular weight 50-100 kDa that inhibited the motility of the highly motile, highly metastatic MAT-LyLu subline.

Bile duct-specific lectins, Dolichos biflorus agglutinin and peanut agglutinin, as probes in mouse hepatocarcinogenesis.

Background: It is well established that alterations in the expression of cell surface glycoproteins occur during the course of tumorigenesis and can be detected immunohistochemically. However, no consistent markers of malignancy in mouse hepatocellular tumors have yet been identified.

Experimental Design: Lectin histochemistry, using three bile duct-specific lectins, Dolichos biflorus agglutinin (DBA), peanut agglutinin (PNA) and soybean agglutinin (SBA), and anti-epidermal keratin immunohistochemistry, was conducted on formalin-fixed, paraffin-embedded tissues of a spectrum of benign and malignant hepatocellular proliferative lesions of mice, including hepatocholangiocarcinomas.

Confocal laser scanning immunofluorescence microscopy of the pulmonary surfactant system. Association of surfactant protein A with the nucleus of the alveolar type II cell.

Background: Localization of surfactant protein A (SP-A) to nucleus of type II cells isolated from the lungs of rats has been reported. Data suggested that most SP-A was located within lamellar bodies of the type II cell; however, some SP-A was found in other cytoplasmic regions of the cell and in particular in the nucleus.

Experimental Design: Type II cells and type II cell nuclei isolated from the lungs of rats were reacted with affinity-purified antibodies against SP-A.

Phenotypic marker expression during fetal and neonatal differentiation of rat tracheal epithelial cells.

The expression of phenotypic markers was examined during fetal and neonatal differentiation of rat tracheal epithelial (RTE) cells. The rat counterpart of human keratin 18 was predominantly found in columnar cells in the adult trachea. It was detected in the primordial tracheal epithelium first seen on gestational day (GD) 12 (term = 21.