Animals sensitized by intratracheal administration of particulate Micropolyspora faeni antigen and subsequently challenged with the antigen intracheally developed lesions of hypersensitivity pneumonitis histologically similar to those observed in man with this disease. Animals sensitized with antigen but depleted of complement with cobra venom factor prior to challenge with the antigen manifested a significant reduction in mean lesion indices when compared to a group of control animals that were not complement-depleted. These data indicate that complement is necessary for the development of pulmonary lesions of experimental hypersensitivity pneumonitis in the rabbit.One hundred and ten children were studied 9 years after each had been in hospital for croup. They were evaluated with a questionnaire, physical examination, allergy skin testing, pulmonary function tests, and a histamine inhalation challenge. Fifty-seven of them had recurrent episodes of croup, and 33 were defined as allergic. The association between allergy and recurrent croup was highly significant. Airways hyper-reactivity was found in 23 of them, and was associated with allergy and recurrent croup. The group of children with a history of recurrent croup could be distinguished from the group with one or two episodes by male predominance, onset of the disease at a younger age, familial predisposition, a significantly greater association with allergy and airways hyper-reactivity, slightly lower expiratory flow rates in pulmonary function tests, and a tendency towards the subsequent development of asthma.
Repeated intratracheal (IT) inoculation of rabbits with a homogenized, saline suspension of Micropolyspora faeni produced bronchopulmonary (BP) histologic lesions resembling those of human hypersensitivity pneumonitis. With an in vitro phagocytic and bactericidal assay, an analysis of BP macrophages from M. faeni-injected rabbits demonstrated activation at both 2 and 4 weeks after the initiation of immunization. No BP macrophage activation was observed in immunized rabbits 6 weeks post-inoculation. BP macrophage activation was capable of recall after 6 weeks in M. faeni-sensitized animals that received a booster IT injection (2 mg) that did not activate “normal” alveolar wash cells. This recall of BP macrophage activation was accompanied by both a marked migration of mononuclear cells into the lung and positive delayed hypersensitivity skin reactions after intradermal injection of M. faeni antigen. Pulmonary histologic examination of sensitized, boosted rabbits suggested an enhanced cellular parenchymal infiltrate when compared with appropriate controls. The above observations confirm the occurrence of immunologically activated BP macrophages in rabbits inoculated with M. faeni via the respiratory tract route and suggest a correlation between macrophage activation and histopathology.
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