Leukotriene B
4 (LTB
4), an arachidonic acid metabolite released by neutrophils, is involved in the regulation of the host immune response to antigenic stimulation. Furthermore, LTB
4 affects the chemokinesis, aggregation, and enzyme release of neutrophils and stimulates activity of cytotoxic T cells, natural killer cells and suppressor T cells.
On the other hand, smoking typically results in inflammatory stimulation of the lung, and long-term smoking can cause chronic stimulation.
In this paper, we report the measurement of LTB
4, IgG, IgA, IgM, IgD and IgE in sera of cigarette smokers who did not have an allergic reaction (group 1), non-smokers who also had no history of allergy (group 2) and non-smokers who had delicate allergic conditions (group 3). The mean LTB
4 concentration in serum of group 1 was nearly 3.3-fold greater than in group 2 and 2-fold greater than in group 3, being 430±55 (Mean±S. D.), 130±22 and 220±14pg/ml, respectively. Concentrations of IgG, IgA, IgM, IgD and IgE of all volunteers were in the normal healthy range. The mean concentration of IgE in the serum of group 1 did not change significantly within one day. It was 35±4IU/ml in the morning, 34±4IU/ml in the afternoon, 31±2IU/ml in the evening and 32±4IU/ml the next morning. But in group 3 the IgE concentration changed significantly within one day, being<25IU/ml in the morning, 97±7IU/ml in the afternoon, 97±7IU/ml in the evening and 25±14IU/ml the next morning. The IgE concentration in the serum of group 2 showed the same tendency as group 3. For all groups the LTB
4 concentration in the serum changed during the day, that is LTB
4 in the afternoon was higher than LTB
4 in the morning. But the LTB
4 in the evening was almost the same as in the morning, and remained so until the next morning.
We also measured nicotine and its metabolites in each volunteer's urine. We could detect nicotine and its metabolite, cotinine in urine of group 1, and a slight quantity of nocotine in urine of group 2 and group 3.
Thus, it appears that the production and release of LTB
4 are promoted by antigens which are inhaled through smoking and that LTB
4 can be increased in serum by passive smoking as can IgE.
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