Considerable effort directed toward designing a safe and effective vaccine for Bordetella pertussis in which the cellular and/or acellular antigens necessary to confer immunity are known has been hampered by lack of information on the pathogenesis of the natural infection. The study presented here describes an animal model of lung infection by B. pertussis encased in agar beads in adult (200- to 220-g) male Sprague-Dawley rats. At 3 and 7 days after inoculation with phase I B. pertussis, organisms could be recovered from the lungs of rats; however, organisms were not recoverable at days 10 and 14 but reappeared in lung homogenates at day 21. Histopathological examination revealed findings similar to those seen in human disease. At day 3, a mild lymphocytic infiltrate was present in the bronchi, with progressive lymphoid hyperplasia peribronchially. By day 7, a necrotizing inflammation of the tracheobronchial mucous membranes, characterized by both mononuclear and polymorphonuclear cells, was noted. Phase III B. pertussis organisms were not recoverable from the lungs of inoculated rats at day 3 after inoculation, nor were histological changes noted in these animals. Clinical findings in phase I B. pertussis-infected rats included hypoglycemia, circulating lymphocytosis, and paroxysms in which air was forcibly expelled from the mouth or nose.
The majority of immunoglobulin in tears is of the immunoglobulin A (IgA) isotype, which is produced mainly by plasma cells of the lacrimal gland. The mechanism responsible for the lodging of the IgA cells in this gland is unknown and probably not dependent on direct glandular encounter with antigen. Previous experiments have suggested that a Th cell from the lacrimal gland can influence B lymphocytes to differentiate into IgA plasma cells. Mechanisms responsible for the IgA-specific Th cell accumulation in the LG could be related to nervous system influences, possibly neuropeptides. These effects on Th cells could be mediated either directly or through lacrimal gland epithelial cells. Such a mechanism could explain the presence of IgA-producing plasma cells in the lacrimal gland, and would allow strategies for manipulation of this important first line defense immune system.
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