With the use of monoclonal antibodies (mAb) and immunohistology, the numbers of phenotypically distinct cells infiltrating lung tissue from 15 postmortem (PM) cases of fatal asthma were quantified and compared with 6 cases of cystic fibrosis (CF) (three postmortem, three transplant) and 10 nonasthmatic cases of sudden death matched for age and sex. Tissue eosinophilia was significantly greater (p less than 0.001) in the fatal asthma group than in the CF or sudden death controls. In asthma, approximately 40% of the eosinophilic infiltrate was EG2 positive (an indication of eosinophil activation and secretion of eosinophil cationic protein). The numbers of eosinophils and EG2 positive cells were significantly elevated in the subjects with acute severe asthma who had had a duration of terminal illness exceeding, as compared with less than, 24 h (p less than 0.05). When compared with the sudden death controls, there were increases in the numbers of Dako L C positive cells (i.e., CD45 positive "total leukocytes") in both fatal asthma and CF (p less than 0.01 and 0.05, respectively). The mean number of MT-1 positive (T) cells in the asthma and CF groups was approximately twice that of the control (p less than 0.05 and 0.01, respectively). The mean number of MB2 positive (B) cells was similar for both the asthma and sudden death control groups but was significantly increased in CF (p less than 0.05). The average T:B cell ratios were 6:1, 1:1, and 2:1 in the fatal asthma, CF, and control groups, respectively. The results support a role for the T lymphocyte in the pathogenesis of fatal asthma and CF.(ABSTRACT TRUNCATED AT 250 WORDS)

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The effects of exposure to hyperoxic conditions (> 95 kPa at normobaric pressure) on bronchial wall dimensions and lung mechanics were examined in adult rats. Measurements of baseline pulmonary resistance and changes in pulmonary resistance following acetylcholine aerosol inhalation were made in rats exposed to hyperoxia for 48 and 60 h and in control rats exposed to air. Exposures for 48 h were carried out in humid (80% relative humidity) or dry (35-40% relative humidity) conditions. Morphometric measurements of airway wall thickness in lobar bronchi were made in separate groups of similarly exposed rats. Exposure to hyperoxia was associated with an increase in baseline pulmonary resistance (control rats 0.043 (0.016) cmH2O ml-1 s-1, 60 h exposed rats 0.125 (0.042) cmH2O ml-1 s-1) but hyper-responsiveness to acetylcholine inhalation did not occur. Thickness of the airway wall and its subdivisions, epithelium, lamina propria and muscularis, was not altered by hyperoxic exposure in humid conditions. However, epithelial thickening in the lobar bronchi was observed in rats exposed for 48 h to hyperoxia in dry conditions compared to rats exposed in humid conditions (mean (SD) thickness 13.2 (3.3) microns for controls, 14.5 (1.5) microns for humid exposed rats and 16.5 (3.3) microns for dry exposed rats). The increase in pulmonary resistance caused by hyperoxic exposure is unlikely to be due to airway damage as airway hyper-responsiveness did not occur, and is more likely to be associated with the development of alveolar oedema. Environmental humidity may modulate lung damage induced by hyperoxia, as exposure in dry conditions was associated with significant epithelial thickening.

Clones of cultivated amniotic fluid cells that have distinct morphologic and growth characteristics (F, AF and E-type) were examined by one-dimensional SDS polyacrylamide gel electrophoresis (SDS-PAGE) and by two-dimensional electrophoresis employing isoelectric focusing and SDS-PAGE (IEF-PAGE). No qualitative differences in band pattern were observed in SDS-PAGE between the various amniotic fluid cell types, but consistent quantitative differences in the ratios of four bands of presumed filamentous proteins provided good distinction between amniotic fluid cells and postnatal skin fibroblast-like cells. By adding separation on the basis of electrical charge to that of molecular size (IEF-PAGE), we observed reproducible qualitative differences in the protein spot patterns between F and both AF and E-type amniotic fluid cells. At least eight discrete proteins appear not be synthesized by prenatal F-type cells in comparison with their isogenic AF and E counterparts under identical culture conditions. The two-dimensional electrophoretic patterns thus confirm that F and AF amniotic cells, in spite of their morphologic and growth kinetic similarities, are developmentally distinct cell types that retain their differentiated states in culture.

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