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Notes: The pathogenesis of summer-type hypersensitivity pneumonitis, which often occurs in Japan, was examined by analysing the cell profile, especially the lymphocyte sub-populations, of bronchoalveolar lavage fluid from these patients: twenty-two normal volunteers and fourteen patients with localized lung cancer as controls. Lymphocyte sub-populations were determined by the micro-testplate method. In the bronchial fluid of the summer hypersensitivity group, the total cell number was much higher (five to ten times) than in the control groups, and the percentage of lymphocytes reached 84-2 + 5.1 (mean + s.e. mean); the percentage of T lymphocytes was significantly increased (95.6 + 1.0), but that of B lymphocytes (3.2 + 0.6) was similar to that of the control groups, though the absolute numbers of B and T lymphocytes were higher than in the control groups. In the peripheral blood of the summer hypersensitivity group, the percentage of B lymphocytes was significantly higher than that found in the normal volunteers, but that of T lymphocytes was not increased. Cellular changes in bronchial fluid were more evident than changes seen by X-ray examination and are considered to be a good parameter of the severity of hypersensitivity pneumonitis. It is considered that cell-mediated immunity as well as the Arthus reaction may be intimately related to the pathogenesis of summer-type hypersensitivity pneumonitis.

Notes: The effect of aprotinin, a plasmin inhibitor, is evaluated in experimental pemphigus. Serum with indirect immunofluorescence IgG litres of 1:1280 was obtained from a pemphigus foliaceus patient. Twenty neonatal Balb-c mice less than 1-day-old were injected intraperitoneally every 24 h with 0·1 ml of pemphigus foliaceus serum. Ten were also inoculated subcutaneously with 0·1 ml physiological saline solution (Group 1), and another ten animals received aprotinin 0·1 ml subcutaneously (Group 2). Five hours later serum and skin samples from the mice were obtained for histological study and indirect and direct immunofluorescence. Clinically extensive disease and histologically subcorneal pemphigus with extensive acantholysis were observed in Group 1. In Group 2 no clinical manifestations were seen apart from minimal acantholysis in four mice. The direct immunofluorescence for intercellular epidermal IgG was positive in both groups. Similar titres of IgG were seen in mouse serum in both groups (1:160-1:320). We conclude that aprotinin is able to inhibit experimental pemphigus in neonatal Balb-c mice by passive transfer of pemphigus foliaceus serum. It also suggests that plasmin plays an important role in the pathophysiology of the experimental disease.Pemphigus is a potentially fatal autoimmune blistering disease. It is characterized by a single autoantibody, pemphigus IgG which binds to a specific antigen belonging to the cell surface of differentiated cells in stratified epithelium of birds and mammals. 1–2The experimental pemphigus model in Balb-c mice, was successfully developed by Anhalt et al. in 1982. 3 They showed that purified IgG from patients with pemphigus vulgaris, injected intraperitoneally in mice, may reproduce pemphigus clinically, histologically, immunologically and ultrastructurally. Since then, other papers have appeared describing the use of the murine experimental model. 4–6Other in vitro studies (epidermal cell cultures) indicate that the IgG of pemphigus vulgaris and pemphigus foliaceus produce a significant increase in plasminogen activator. Hashimoto et al.7 reported that an increase in the activity of plasminogen activator could be an important step in the development of acantholysis after the reaction of pemphigus IgG with antigen. Plasminogen activator would act on the plasminogen of the epidermis generating plasmin, which would degrade the adhesive components of the cell surface. The addition of corticosteroids to epidermal cell cultures, incubated with pemphigus autoantibodies inhibited the increase of plasminogen activator significantly but failed to block the acantholytic process. 8 In other studies inhibition of acantholysis was obtained. 9If plasmin inhibitors such as lima bean trypsin inhibitor and aprotinin, which do not inhibit plasminogen activator, are added to cell cultures treated with pemphigus immunoglobulins, acantholysis is not produced. These findings, are consistent with the theory that plasmin is the enzyme that produces acantholysis in pemphigus. 10The present study attempts to evaluate the in vivo effect of a plasmin inhibitor such as aprotinin. To our knowledge this problem has not been investigated in the murine model of the disease.