Delayed Hypersensitivity to Beryllium Compounds

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Abstract
Assessment of delayed hypersensitivity to beryllium compounds was made by using in vivo and in vitro techniques in sensitized and normal guinea pigs. Hartley strain guinea pigs could be sensitized by repeated intradermal injections over a 6-week period, but not by single injections of beryllium intraperitoneally or intramuscularly. Maximum subtoxic doses of BeSO4 (5 µg) and BeF2 (2.5 µg) were determined for the intradermal skin test in normal guinea pigs. When these doses of salts were used to challenge sensitized animals, classical delayed hypersensitive skin reactions ensued. When normal and sensitized guinea pigs were challenged with an insoluble form of beryllium (BeO), the reactions obtained were considered typical of classical beryllium granulomata in only the sensitized animals. Soluble mediators of cellular hypersensitivity were assayed as in vitro correlates of delayed hypersensitivity. There was a 74% positive correlation of migration-inhibitory factor (MIF) and skin test results in sensitized animals. This sensitivity to beryllium was transferable by cells when assessed by both in vivo and in vitro techniques in the passively sensitized recipients. Lymphocytotoxin was also demonstrable in cell suspensions from sensitized animals when exposed to beryllium, but not in unsensitized controls. Patients with diagnosed chronic pulmonary berylliosis were assessed for sensitivity by in vitro inhibition of peripheral blood leukocyte migration and showed MIF production when exposed to BeSO4 in vitro. An unexplained inhibition of leukocyte migration was observed when peripheral leukocytes from these patients were exposed in vitro to tuberculin purified protein derivative (PPD), even though the patients were all skin test-negative before steroid therapy. Peripheral blood leukocytes from patients with chronic lung disease other than berylliosis and no history of exposure to beryllium were MIF-negative to BeSO4, but positive to PPD. The available data support the hypothesis that reactivity to beryllium compounds is due to classical delayed hypersensitivity, and the techniques that were used may be applicable as diagnostic tools.

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