ABSTRACT
Figure 3 Photomicrographs of an airway from a child who died of acute adenoviral bronchiolitis. Note the extensive epithelial cell necrosis and sloughing of inflammatory exudate into the lumen at center (A). In situ hybridization of a serial section with a nonisotopic probe (B) reveals large amounts of adenoviral genome (dark dots) within the nuclei of infected epithelial cells. (From Ref. 46.)
of biochemical and biomechanical events involving cell membranes stimulate the production of membrane-derived mediators, including the prostaglandins and leukotrienes. Many of these mediators modulate smooth muscle activity and influence airways caliber by the mechanisms described above. A further consequence of viral-induced epithelial cell injury is decreased production of neutral endopeptidase ( 17), an enzyme important for the metabolism of a wide variety of bronchoconstricting neuropeptides, which increase mucus secretion from both the goblet cells and submucosal glands. Moreover, the loss of an intact epithelial barrier from acute viral infection results in exposure of submucosal afferent nerve endings to physical, chemical, biological, and environmental agents that stimulate neurogenic inflammation mediated by peptides such as neurokinin A and substance P.
