Suppression of polyclonal B cell activation in scrapie-infected C3H/HeJ mice.

A consistent modification in B lymphocyte activation has been observed 1 month after infection of C3H/HeJ mice with scrapie. The mitogenic response to lipopolysaccharide of splenocyte cultures from experimental mice was reduced 30 to 60% as compared to controls. This reduction in mitogen responsiveness was transient but coincided with the onset of detectable splenomegaly and with the reported recovery of maximum yield of infectious scrapie agent in the spleen. The DNA synthetic response to lipopolysaccharide stimulation of splenocytes from scrapie-infected C3H/HeJ mice was depressed relative to controls only between 20 and 40 days after intracerebral inoculation. At all other times, experimental and control responses were identical. Scrapie-associated decreases in mitogenesis were found whether the spleen cell cultures contained splenocytes from individual mice, splenocytes pooled from several mice, or gradient-purified mononuclear cells. The responses of C3H/HeJ splenocyte cultures to phytohemagglutinin or concanavalin A stimulation were unaffected by scrapie infection.

Pulmonary changes induced by low-level ozone: morphological observations.

This study defines the surface and ultrastructural changes which occur in mouse lungs during the early stages of continuous low-level ozone exposure. Swiss-Webster mice were exposed for 35 consecutive days to 0.5 ppm ozone, a level of oxidant gas which simulates levels occurring during an episode of severe smog in urban areas of the California south coast air basin. Groups of mice were killed on day 7, 21, or 35 of exposure and their lungs excised and examined by light microscopy, scanning electron microscopy, and transmission electron microscopy. Lung damage was most severe at the transition zone from terminal bronchiole to alveolar duct. This centriacinar lesion consisted of (1) increased numbers of macrophages within proximal alveoli of alveolar ducts, (2) clusters of type 2 pneumonocytes lining these proximal alveoli, (3) changes in surface characteristics of Clara cells, and (4) hyperplastic nodules of bronchiolar epithelium within terminal bronchioles. Inflammatory cell infiltrates were reduced in numbers at 35 days of exposure as compared to 7 days of exposure, but the hyperplastic bronchiolar epithelium persisted and, in fact, increased in severity as exposure length increased. Although inflammatory cell infiltrates were observed in proximal alveoli of alveolar ducts, the hyperplastic bronchiolar epithelial changes were observed throughout the lengths of terminal bronchioles examined. The variability in response to ozone insult of nonciliated cells in the terminal bronchiole of rats, mice, and monkeys is discussed.