No abstract

No abstract

Age-related changes in lung structure and function were investigated in murine models of accelerated senescence (SAM-P/1) and of normal aging (SAM-R/1). In morphometric studies, most of the parameters examined, including lung volume, mean linear intercept, total alveolar duct air volume, and total alveolar air volume, began to increase and the internal surface area per unit lung volume and total elastic fiber length per unit lung volume began to decrease from 2 months of age, and these changes continued to progress up to 10 months of age in SAM-P/1. In SAM-R/1, there were no significant changes in these parameters from 2 to 6 months of age, thereafter slight but steady changes were observed up to 25 months of age. Thus, significant differences in these parameters between SAM-P/1 and SAM-R/1 became evident in mice 6 to 17 months of age. Internal surface area and total elastic fiber length showed no age-related changes after 2 months of age, and total alveolar air volume showed no age-related changes after 6 months of age in either strain. All morphometric parameters examined showed similar levels at 17 months of age in SAM-P/1 and 25 months of age in SAM-R/1. Histologic observations revealed no evidence of destruction of the alveolar wall or elastic fibers in the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

A low molecular weight (MW) protein was isolated from the bronchoalveolar lavage fluid of a patient with alveolar proteinosis. The protein was isolated on DEAE-cellulose and CM-cellulose columns by a cross-reaction with the monoclonal antibody against pig low MW protein (15 kDa) used as a marker. Acidic ethanol-soluble proteins obtained from the fractions eluted by 0.09 to 0.16 M NaCl concentration from the CM-cellulose column migrated mainly as a 15-kDa band in the SDS-PAGE system without urea but mainly as a 5-kDa band in a system with 8 M urea. The isoelectric point of the protein was pH 10 to 11, and it contained a large proportion of hydrophobic amino acids (72%), especially leucine (17%). The arginine content was also high (9%). Two monoclonal antibodies were raised against this low MW protein, and immunohistochemical studies revealed that the antigen was located in the inclusions of alveolar wall cells in normal lungs and in lungs from a patient with alveolar proteinosis. These results indicate that the low MW protein originates from lamellar inclusions of alveolar wall cells (possibly type II epithelial cells) and is secreted into alveolar spaces.