Lh. Youkeles et al., DECREASED TOBACCO-GLYCOPROTEIN-INDUCED LYMPHOCYTE-PROLIFERATION IN-VITRO IN PULMONARY EOSINOPHILIC GRANULOMA, American journal of respiratory and critical care medicine, 151(1), 1995, pp. 145-150
Citations number
36
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
Pulmonary eosinophilic granuloma is a disorder caused by localized col
lections of proliferating histiocytes in the lung. Little is known abo
ut its etiology except that the majority (58 to 97%) of patients are c
urrent or ex-smokers, making the potential etiologic role of tobacco p
roducts an important area for research. Tobacco glycoprotein (TGP) is
a potent immunostimulator that has been isolated from cigarette smoke.
TOP-specific lymphocyte proliferation, and cytokine production in vit
ro, were measured in three patients with pulmonary eosinophilic granul
oma in remission and in three closely matched normal subjects with sim
ilar smoking histories. One patient with eosinophilic granuloma of bon
e and a matched control subject were also studied. Peripheral blood mo
nonuclear cells were cultured with TGP, tile recall antigen streptokin
ase (SK), and the mitogen concanavalin A (Con A). All three of the pat
ients with pulmonary eosinophilic granuloma exhibited significant decr
eases 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 respo
nses 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 a
ssayed for cytokine levels (IL-l, IL-2, and IL-6). TOP-stimulated IL-2
production was significantly lower in the patients with pulmonary eos
inophilic granuloma than in the normal subjects, confirming the reduce
d T-cell proliferative response. TG was found to be a very potent indu
cer of IL-1 and IL-2, but there was no difference between patients and
control subjects. These findings demonstrate that the lymphocyte prol
iferation response of patients with pulmonary eosinophilic granuloma t
o TGP is significantly different from the response of normal subjects
or cigarette smokers without this disease, and they suggest that an al
tered immune response to TGP may be involved in the pathogenesis of th
e disease. However, the exact mechanisms by which tobacco might induce
pulmonary eosinophilic granuloma remain to be established.