Pulmonary eosinophilic granuloma is a disorder caused by localized collections of proliferating histiocytes in the lung. Little is known about its etiology except that the majority (58 to 97%) of patients are current or ex-smokers, making the potential etiologic role of tobacco products an important area for research. Tobacco glycoprotein (TGP) is a potent immunostimulator that has been isolated from cigarette smoke. TGP-specific lymphocyte proliferation, and cytokine production in vitro, were measured in three patients with pulmonary eosinophilic granuloma in remission and in three closely matched normal subjects with similar smoking histories. One patient with eosinophilic granuloma of bone and a matched control subject were also studied. Peripheral blood mononuclear cells were cultured with TGP, the recall antigen streptokinase (SK), and the mitogen concanavalin A (Con A). All three of the patients with pulmonary eosinophilic granuloma exhibited significant decreases in lymphocyte stimulation to TGP, despite normal responses to SK and Con A. In contrast, the response of the patient with eosinophilic granuloma of bone was higher than her matched control. The mean responses of the patients with pulmonary eosinophilic granuloma to TGP was significantly lower than the mean of nondiseased smokers or of normal nonsmokers. Twenty-four-hour culture supernatants were collected and assayed for cytokine levels (IL-1, IL-2, and IL-6). TGP-stimulated IL-2 production was significantly lower in the patients with pulmonary eosinophilic granuloma than in the normal subjects, confirming the reduced T-cell proliferative response.(ABSTRACT TRUNCATED AT 250 WORDS)

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Sixty-three adults with symptomatic chronic rhinosinusitis had computerized tomographic (CT) scans of the paranasal sinuses, which were used to quantify disease severity. These patients were divided into three closely age- and sex-matched groups: a CT scan-negative group (chronic rhinitis only), a mild sinusitis group and a severe sinusitis group. Serum dust mite-specific IgG levels were found to be significantly elevated in the sinusitis patients compared with a matched group of asymptomatic normal individuals. Levels were highest in the more severe sinusitis group, in which the mean titre was 559 U/ml and the incidence of titres greater than 400 U/ml was 48%, as compared with a mean titre of 139 U/ml and only a 10% incidence of titres greater than 400 U/ml in the normal subjects (P < 0.005 and < 0.01). In contrast, although the frequency of immediate hypersensitivity to dust mite, as assessed by intradermal skin tests, tended to be higher in patients with sinusitis, it was not significantly different from normal individuals. The association between mite IgG and disease was most striking in the patient sub-group with negative mite skin tests. In this group, mite IgG levels were significantly higher than normal, even in those patients with only chronic rhinitis. These findings demonstrate that increased serum levels of IgG against dust mites are strongly associated with chronic rhinosinusitis, especially in the sub-group of patients who are not allergic to mites.

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Twenty-four asthmatic patients were evaluated for the presence of circulating cytotoxic lung antibodies. These patients were further classified as either extrinsic or intrinsic asthmatics on the basis of skin testing, age of onset, and atopic history. Of the 12 patients considered to have extrinsic asthma, 10 had positive titers, one borderline, and one negative for cytotoxic lung antibodies. In the group of 12 patients classified as intrinsic asthmatics, eight had negative titers, two borderline, and two positive for cytotoxic lung antibodies. Adsorption studies indicated that these antibodies were organ-specific. Twenty normal non-smoking controls were also tested, all of whom were negative. Five patients with allergic rhinitis, positive intradermal skin tests, and no history of asthma were found to be negative for cytotoxic lung antibodies.

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